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Gene expression signature in organized and growth-arrested mammary acini predicts good outcome in breast cancer. | S1 (immortal nonmalignant) HMECs on successive days after seeding in a lrECM assay. Both HMECs underwent growth arrest in G0-G1 and differentiated into polarized acini between days 5 and 7. We identified gene expression changes with the same temporal pattern in both lines and examined the expression of these genes in a previously published panel of microarray data for 295 breast cancer samples. We show that genes that are significantly lower in the organized; growth-arrested HMEC than in their proliferatin | 16849555 | [
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Gene expression signature in organized and growth-arrested mammary acini predicts good outcome in breast cancer. | g counterparts can be used to classify breast cancer patients into poor and good prognosis groups with high accuracy. This study represents a novel unsupervised approach to identifying breast cancer markers that may be of use clinically. | 16849555 | [
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Proepithelin promotes migration and invasion of 5637 bladder cancer cells through the activation of ERK1/2 and the formation of a paxillin/FAK/ERK complex. | The growth factor proepithelin (also known as progranulin; acrogranin; PC-derived growth factor; or granulin-epithelin precursor) is a secreted glycoprotein that functions as an important regulator of cell growth; migration; and transformation. Proepithelin is overexpressed in a great variety of cancer cell lines and clinical specimens of breast; ovarian; and renal cancer as well as glioblastomas. In this study; we have investigated the effects of proepithelin on bladder cancer cells using human recombinant | 16849556 | [
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Proepithelin promotes migration and invasion of 5637 bladder cancer cells through the activation of ERK1/2 and the formation of a paxillin/FAK/ERK complex. | proepithelin purified to homogeneity from 293-EBNA cells. Although proepithelin did not appreciably affect cell growth; it did promote migration of 5637 bladder cancer cells and stimulate in vitro wound closure and invasion. These effects required the activation of the mitogen-activated protein kinase pathway and paxillin; which upon proepithelin stimulation formed a complex with focal adhesion kinase and active extracellular signal-regulated kinase. Our results provide the first evidence for a role of pro | 16849556 | [
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Proepithelin promotes migration and invasion of 5637 bladder cancer cells through the activation of ERK1/2 and the formation of a paxillin/FAK/ERK complex. | epithelin in stimulating migration and invasion of bladder cancer cells; and support the hypothesis that this growth factor may play a critical role in the establishment of the invasive phenotype. | 16849556 | [
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RRIG1 mediates effects of retinoic acid receptor beta2 on tumor cell growth and gene expression through binding to and inhibition of RhoA. | The expression of retinoic acid receptor beta2 (RAR-beta2) is frequently lost in various cancers and their premalignant lesions. However; the restoration of RAR-beta2 expression inhibits tumor cell growth and suppresses cancer development. To understand the molecular mechanisms responsible for this RAR-beta2-mediated antitumor activity; we did restriction fragment differential display-PCR and cloned a novel retinoid receptor-induced gene 1 (RRIG1); which is differentially expressed in RAR-beta2-positive and | 16849557 | [
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RRIG1 mediates effects of retinoic acid receptor beta2 on tumor cell growth and gene expression through binding to and inhibition of RhoA. | RAR-beta2-negative tumor cells. RRIG1 cDNA contains 2;851 bp and encodes a protein with 276 amino acids; the gene is localized at chromosome 9q34. Expressed in a broad range of normal tissues; RRIG1 is also lost in various cancer specimens. RRIG1 mediates the effect of RAR-beta2 on cell growth and gene expression (e.g.; extracellular signal-regulated kinase 1/2 and cyclooxygenase-2). The RRIG1 protein is expressed in the cell membrane and binds to and inhibits the activity of a small GTPase RhoA. Whereas i | 16849557 | [
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RRIG1 mediates effects of retinoic acid receptor beta2 on tumor cell growth and gene expression through binding to and inhibition of RhoA. | nduction of RRIG1 expression inhibits RhoA activation and f-actin formation and consequently reduces colony formation; invasion; and proliferation of esophageal cancer cells; antisense RRIG1 increases RhoA activity and f-actin formation and thus induces the colony formation; invasion; and proliferation of these cells. Our findings therefore show a novel molecular pathway involving RAR-beta2 regulation of RRIG1 expression and RRIG1-RhoA interaction. An understanding of this pathway may translate into better | 16849557 | [
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RRIG1 mediates effects of retinoic acid receptor beta2 on tumor cell growth and gene expression through binding to and inhibition of RhoA. | control of human cancer. | 16849557 | [
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Papilloma development is delayed in osteopontin-null mice: implicating an antiapoptosis role for osteopontin. | Osteopontin is a secreted; adhesive glycoprotein; whose expression is markedly elevated in several types of cancer and premalignant lesions; implicating its association with carcinogenesis. To test the hypothesis that induced osteopontin is involved in tumor promotion in vivo; osteopontin-null and wild-type (WT) mice were subjected to a two-stage skin chemical carcinogenesis protocol. Mice were initiated with 7;12-dimethylbenz(a)anthracene (DMBA) applied on to the dorsal skin followed by twice weekly applic | 16849558 | [
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Papilloma development is delayed in osteopontin-null mice: implicating an antiapoptosis role for osteopontin. | ation of 12-O-tetradecanoylphorbol-13-acetate (TPA) for 27 weeks. Osteopontin-null mice showed a marked decrease both in tumor/papilloma incidence and multiplicity compared with WT mice. Osteopontin is minimally expressed in normal epidermis; but on treatment with TPA its expression is highly induced. To determine the possible mechanism(s) by which osteopontin regulates tumor development; we examined cell proliferation and cell survival. Epidermis from osteopontin-null and WT mice treated with TPA thrice or | 16849558 | [
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Papilloma development is delayed in osteopontin-null mice: implicating an antiapoptosis role for osteopontin. | with DMBA followed by TPA for 11 weeks showed a similar increase in epidermal hyperplasia; suggesting that osteopontin does not mediate TPA-induced cell proliferation. Bromodeoxyuridine staining of papillomas and adjacent epidermis showed no difference in cell proliferation between groups. However; terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling analyses indicated a greater number of apoptotic cells in DMBA-treated skin and papillomas from osteopontin-null versus WT mice. These studie | 16849558 | [
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Papilloma development is delayed in osteopontin-null mice: implicating an antiapoptosis role for osteopontin. | s are the first to show that induction of the matricellular protein osteopontin facilitates DMBA/TPA-induced cutaneous carcinogenesis most likely through prevention of apoptosis. | 16849558 | [
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Prx1 suppresses radiation-induced c-Jun NH2-terminal kinase signaling in lung cancer cells through interaction with the glutathione S-transferase Pi/c-Jun NH2-terminal kinase complex. | Radiotherapy is one of the major treatment modalities for lung cancer. Cell killing by ionizing radiation is mediated primarily through the reactive oxygen species (ROS) and ROS-driven oxidative stress. Prx1; a peroxiredoxin family member; was shown to be frequently elevated in lung cancer cells and tissues. Although the antioxidant function of Prx1 is expected to affect the radiotherapy response of lung cancer; the physiologic significance of its peroxidase activity in irradiated cells is unclear because t | 16849559 | [
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Prx1 suppresses radiation-induced c-Jun NH2-terminal kinase signaling in lung cancer cells through interaction with the glutathione S-transferase Pi/c-Jun NH2-terminal kinase complex. | he catalytic Cys52 is easily inactivated by ROS due to its overoxidation to sulfinic or sulfonic acid. In this study; we investigated the role of Prx1 in radiation sensitivity of human lung cancer cells; with special emphasis on the redox status of the catalytic Cys52. We found that overexpression of Prx1 enhances the clonogenic survival of irradiated cells and suppresses ionizing radiation-induced c-Jun NH2-terminal kinase (JNK) activation and apoptosis. The peroxidase activity of Prx1; however; is not ess | 16849559 | [
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Prx1 suppresses radiation-induced c-Jun NH2-terminal kinase signaling in lung cancer cells through interaction with the glutathione S-transferase Pi/c-Jun NH2-terminal kinase complex. | ential for inhibiting JNK activation. The latter effect is mediated through its association with the glutathione S-transferase pi (GSTpi)-JNK complex; thereby preventing JNK release from the complex. Reduced JNK activation is observed when the peroxidase activity of Prx1 is compromised by Cys52 overoxidation or in the presence of the Cys52 to Ser52 mutant (Prx1C52S) lacking peroxidase activity. We show that both Prx1 and Prx1C52S interact with the GSTpi-JNK complex and suppress the release of JNK from the c | 16849559 | [
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Prx1 suppresses radiation-induced c-Jun NH2-terminal kinase signaling in lung cancer cells through interaction with the glutathione S-transferase Pi/c-Jun NH2-terminal kinase complex. | omplex. Our study provides new insight into the antiapoptotic function of Prx1 in modulating radiosensitivity and provides the impetus to monitor the influence of Prx1 levels in the management of lung cancer. | 16849559 | [
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High levels of dioxin-like potential in cigarette smoke evidenced by in vitro and in vivo biosensing. | Cigarette smoke contains low levels of agonists for the aryl hydrocarbon receptor (AhR; also called the dioxin receptor). However; little is understood about the whole potential of cigarette smoke for activating AhR. In this report; we evaluated the total "dioxin-like" activity of cigarette smoke using in vitro and in vivo reporter systems. Cigarette smoke extract (CSE) was prepared from seven cigarette brands (1-20 mg tar content) and subjected to in vitro bioassay based on the xenobiotic-responsive elemen | 16849560 | [
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High levels of dioxin-like potential in cigarette smoke evidenced by in vitro and in vivo biosensing. | t (XRE) as the sensor and secreted alkaline phosphatase (SEAP) as the reporter. Exposure of reporter cells to CSE triggered activation of XRE in a dose-dependent manner; which was suppressed by functional inhibition of AhR. Direct; brief exposure of the cells to cigarette smoke similarly induced activation of XRE. Using 2;3;7;8-tetrachlorodibenzo-p-dioxin (2;3;7;8-TCDD) as the standard; the XRE-activating potential (XAP) of individual smoke was evaluated quantitatively. Positive correlation was observed bet | 16849560 | [
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High levels of dioxin-like potential in cigarette smoke evidenced by in vitro and in vivo biosensing. | ween the tar content and XAP values. The XAP values estimated were extremely high with a range from 18.5 to 51.2 ng 2;3;7;8-TCDD equivalent per cigarette. To further estimate XAP of cigarette smoke in vivo; we generated transgenic reporter mice that secrete SEAP under the control of XRE. After exposure of the mice to smoke; serum levels of SEAP were significantly elevated within 12 hours; peaked at 24 hours; and declined thereafter. These results evidenced for the first time that cigarette smoke has unexpec | 16849560 | [
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Absence of the full-length breast cancer-associated gene-1 leads to increased expression of insulin-like growth factor signaling axis members. | The breast cancer-associated gene-1 (BRCA1) plays many important functions in multiple biological processes/pathways. Mice homozygous for a targeted deletion of full-length BRCA1 (Brca1Delta11/Delta11) display both increased tumorigenesis and premature aging; yet molecular mechanisms underlying these defects remain elusive. Here; we show that Brca1 deficiency leads to increased expression of several insulin-like growth factor (IGF) signaling axis members in multiple experimental systems; including BRCA1-def | 16849561 | [
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Absence of the full-length breast cancer-associated gene-1 leads to increased expression of insulin-like growth factor signaling axis members. | icient mice; primary mammary tumors; and cultured human cells. Furthermore; we provide evidence that activation of IGF signaling by BRCA1 deficiency can also occur in a p53-independent fashion. Our data indicate that BRCA1 interacts with the IRS-1 promoter and inhibits its activity that is associated with epigenetic modification of histone H3 and histone H4 to a transcriptional repression chromatin configuration. We further show that BRCA1-deficient mammary tumor cells exhibit high levels of IRS-1; and acut | 16849561 | [
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Absence of the full-length breast cancer-associated gene-1 leads to increased expression of insulin-like growth factor signaling axis members. | e suppression of Irs-1 using RNA interference significantly inhibits growth of these cells. Those observations provide a molecular insight in understanding both fundamental and therapeutic BRCA1-associated tumorigenesis and aging. | 16849561 | [
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Survival response to B-cell receptor ligation is restricted to progressive chronic lymphocytic leukemia cells irrespective of Zap70 expression. | Despite very similar gene expression profiles; the clinical course of B-cell chronic lymphocytic leukemia (B-CLL) is heterogeneous. Immunoglobulin VH (IgVH) mutational status and expression of B-cell receptor (BCR) signaling mediators have been associated with disease progression. However; the consequences of BCR engagement on cell survival and evolution of the disease remain unclear. We show here that B-CLL cell survival is dependent on the threshold of BCR stimulation induced by immobilized antibody; in c | 16849562 | [
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Survival response to B-cell receptor ligation is restricted to progressive chronic lymphocytic leukemia cells irrespective of Zap70 expression. | ontrast to soluble anti-mu F(ab)'2 antibody; which leads to apoptosis. Measurement of metabolic activity and apoptotic response discriminated two subgroups. "Nonresponders" showed low metabolic activity and unmodified apoptotic response upon BCR stimulation. In contrast; "responders" exhibited increased metabolic activity and inhibition of spontaneous apoptosis. This survival advantage was associated to a BCR-dependent activation profile leading to induction of cyclin D2/cyclin-dependent kinase 4 (cdk4) exp | 16849562 | [
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Survival response to B-cell receptor ligation is restricted to progressive chronic lymphocytic leukemia cells irrespective of Zap70 expression. | ression and G1 cell cycle progression. The ability to respond to BCR ligation correlated with an unfavorable clinical course and allowed to define an additional group of patients among IgVH-mutated cases exhibiting a risk of progression. Remarkably; we show that Zap70 expression was neither mandatory nor sufficient to generate downstream survival signals and cyclin D2/cdk4 up-regulation. In conclusion; BCR engagement has a significant effect on B-CLL cell survival; activation; and G1 progression. Furthermor | 16849562 | [
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Survival response to B-cell receptor ligation is restricted to progressive chronic lymphocytic leukemia cells irrespective of Zap70 expression. | e; our results provide new insights in the physiopathology of progressive IgVH-mutated cases. | 16849562 | [
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The human orthologue of Drosophila ecdysoneless protein interacts with p53 and regulates its function. | Biochemical mechanisms that control the levels and function of key tumor suppressor proteins are of great interest as their alterations can lead to oncogenic transformation. Here; we identify the human orthologue of Drosophila melanogaster ecdysoneless (hEcd) as a novel p53-interacting protein. Overexpression of hEcd increases the levels of p53 and enhances p53 target gene transcription whereas hEcd knockdown has the opposite effects on p53 levels and target gene expression. Furthermore; hEcd interacts with | 16849563 | [
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The human orthologue of Drosophila ecdysoneless protein interacts with p53 and regulates its function. | murine double minute-2 and stabilizes p53 by inhibiting murine double minute-2-mediated degradation of p53. Thus; hEcd protein represents a novel regulator of p53 stability and function. Our studies also represent the first demonstration of a biochemical function for hEcd protein and raise the possibility that altered hEcd levels and/or function may contribute to oncogenesis. | 16849563 | [
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Chemokine (C-C motif) ligand 2 mediates the prometastatic effect of dysadherin in human breast cancer cells. | Dysadherin; a cancer-associated membrane glycoprotein; down-regulates E-cadherin and promotes cancer metastasis. This study examined the role of dysadherin in breast cancer progression. Expression of dysadherin was found to be highest in breast cancer cell lines and tumors that lacked the estrogen receptor (ER). Knockdown of dysadherin caused increased association of E-cadherin with the actin cytoskeleton in breast cancer cell lines that expressed E-cadherin. However; knockdown of dysadherin could still sup | 16849564 | [
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Chemokine (C-C motif) ligand 2 mediates the prometastatic effect of dysadherin in human breast cancer cells. | press cell invasiveness in cells that had no functional E-cadherin; suggesting the existence of a novel mechanism of action. Global gene expression analysis identified chemokine (C-C motif) ligand 2 (CCL2) as the transcript most affected by dysadherin knockdown in MDA-MB-231 cells; and dysadherin was shown to regulate CCL2 expression in part through activation of the nuclear factor-kappaB pathway. The ability of dysadherin to promote tumor cell invasion in vitro was dependent on the establishment of a CCL2 | 16849564 | [
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Chemokine (C-C motif) ligand 2 mediates the prometastatic effect of dysadherin in human breast cancer cells. | autocrine loop; and CCL2 secreted by dysadherin-positive tumor cells also promoted endothelial cell migration in a paracrine fashion. Finally; experimental suppression of CCL2 in MDA-MB-231 cells reduced their ability to metastasize in vivo. This study shows that dysadherin has prometastatic effects that are independent of E-cadherin expression and that CCL2 could play an important role in mediating the prometastatic effect of dysadherin in ER-negative breast cancer. | 16849564 | [
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Generation of replication-dependent double-strand breaks by the novel N2-G-alkylator S23906-1. | S23906-1; a new DNA alkylating agent that reacts with the exocyclic 2-NH2 group of guanine residues yielding monofunctional adducts; is currently under clinical evaluation in phase I trials. To investigate the mechanism of action of S23906-1; we compared parental KB-3-1 cells and KB/S23-500 cells that are 15-fold resistant to S23906-1. Cell death induced by 1 micromol/L S23906-1 in KB-3-1 cells was associated with their irreversible arrest in the G2-M phases of the cell cycle followed by apoptosis; whereas | 16849567 | [
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Generation of replication-dependent double-strand breaks by the novel N2-G-alkylator S23906-1. | a proportion of the resistant KB/S23-500 cells were able to exit from the G2 arrest and divide; leading to a significantly lower rate of apoptosis. The attenuated apoptotic response was associated with decreased Chk2 protein phosphorylation; indicating that the DNA damage signaling pathways are more potently activated in the sensitive cells. However; similar rates of adduct formation and repair were measured in both cell lines. Exposure to S23906-1 induced a higher formation of DNA breaks; measured by the c | 16849567 | [
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Generation of replication-dependent double-strand breaks by the novel N2-G-alkylator S23906-1. | omet assay; in sensitive cells. In agreement; a histone H2AX phosphorylation assay revealed that S23906-1 induced double-strand breaks (DSB) in a dose- and time-dependent manner and that these were more persistent in the parental cells. These DSBs were found mainly in S-phase cells and inhibited by aphidicolin; suggesting that they are DNA replication-mediated DSBs. These results suggest that secondary DNA lesions play an important role in the cytotoxicity of this compound and make histone H2AX phosphorylat | 16849567 | [
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Generation of replication-dependent double-strand breaks by the novel N2-G-alkylator S23906-1. | ion an attractive marker for monitoring the efficacy of S23906-1. | 16849567 | [
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Oncolytic capacity of attenuated replicative semliki forest virus in human melanoma xenografts in severe combined immunodeficient mice. | Oncolytic viruses have gained attention as a novel form of cancer treatment. Many viral vectors in use today have been rendered safe by deletion of genes encoding viral structural proteins; thus making them unable to spread beyond the first infected cells. Hence; such replication-deficient constructs may lack efficacy. Here; we analyzed the oncolytic potential of the replication-competent vector VA7-EGFP; based on the avirulent Semliki Forest virus (SFV) strain A7(74); to kill cancer cells in culture as wel | 16849565 | [
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Oncolytic capacity of attenuated replicative semliki forest virus in human melanoma xenografts in severe combined immunodeficient mice. | l as to target s.c. human melanoma xenografts in severe combined immunodeficient (SCID) mice. VA7-EGFP was able to infect most cancer cell lines studied; leading to complete lysis of the cells within 72 hours after infection. In SCID mice grafted with A2058 human melanoma; marked regression of the xenografts was observed following a single injection of 10(6) plaque-forming units of virus given either i.p.; i.v.; or intratumorally. Histologic analysis revealed the presence of virus not only in all treated tu | 16849565 | [
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Oncolytic capacity of attenuated replicative semliki forest virus in human melanoma xenografts in severe combined immunodeficient mice. | mors but also in the brains of the treated mice; causing progressing neuropathology beginning at day 16 after infection. Following initial oncolysis; clusters of viable tumor cells were observed embedded in connective tissue; and at later stages; encapsulated tumor nodules had formed. Infection of melanoma cells from explant cultures of these nodules revealed that a portion of the cells were resistant to virus. To be eligible for use in virotherapy; the ability of avirulent SFV to spread within tumor tissue | 16849565 | [
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Oncolytic capacity of attenuated replicative semliki forest virus in human melanoma xenografts in severe combined immunodeficient mice. | may have to be improved and the biological safety of the virus may have to be addressed thoroughly in higher animals. | 16849565 | [
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Differential binding of plasminogen, plasmin, and angiostatin4.5 to cell surface beta-actin: implications for cancer-mediated angiogenesis. | Angiostatin4.5 (AS4.5) is the product of plasmin autoproteolysis and consists of kringles 1 to 4 and approximately 85% of kringle 5. In culture; cancer cell surface globular beta-actin mediates plasmin autoproteolysis to AS4.5. We now show that plasminogen binds to prostate cancer cells and that the binding colocalizes with surface beta-actin; but AS4.5 does not bind to the cell surface. Plasminogen and plasmin bind to immobilized beta-actin similarly; with a Kd of approximately 140 nmol/L. The binding is i | 16849568 | [
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Differential binding of plasminogen, plasmin, and angiostatin4.5 to cell surface beta-actin: implications for cancer-mediated angiogenesis. | nhibited by epsilon-aminocaproic acid (epsilonACA); indicating the requirement for a lysine-kringle domain interaction. Using a series of peptides derived from beta-actin in competitive binding studies; we show that the domain necessary for plasminogen binding is within amino acids 55 to 69 (GDEAQSKRGILTLKY). Substitution of Lys61 or Lys68 with arginine results in the loss of the ability of the peptide to block plasminogen binding; indicating that Lys61 and Lys68 are essential for plasminogen binding. Other | 16849568 | [
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Differential binding of plasminogen, plasmin, and angiostatin4.5 to cell surface beta-actin: implications for cancer-mediated angiogenesis. | actin peptides; including peptides with lysine; did not inhibit the plasminogen-actin interaction. AS4.5 did not bind actin at concentrations up to 40 micromol/L. Plasminogen; plasmin; and AS4.5 all contain kringles 1 to 4; however; kringle 5 is truncated in AS4.5. Isolated kringle 5 binds to actin; suggesting intact kringle 5 is necessary for plasminogen and plasmin to bind to cell surface beta-actin; and the truncated kringle 5 in AS4.5 results in its release from beta-actin. These data may explain the m | 16849568 | [
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Inhibition of the multidrug-resistant phenotype by targeting YB-1 with a conditionally oncolytic adenovirus: implications for combinatorial treatment regimen with chemotherapeutic agents. | Bearing in mind the limited success of available treatment modalities for the therapy of multidrug-resistant tumor cells; alternative and complementary strategies need to be developed. It is known that the transcriptional activation of genes; such as MDR1 and MRP1; which play a major role in the development of a multidrug-resistant phenotype in tumor cells; involves the Y-box protein YB-1. Thus; YB-1 is a promising target for new therapeutic approaches to defeat multidrug resistance. In addition; it has bee | 16849566 | [
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Inhibition of the multidrug-resistant phenotype by targeting YB-1 with a conditionally oncolytic adenovirus: implications for combinatorial treatment regimen with chemotherapeutic agents. | n reported previously that YB-1 is an important factor in adenoviral replication because it activates transcription from the adenoviral E2-late promoter. Here; we report that an oncolytic adenovirus; named Xvir03; expressing the viral proteins E1B55k and E4orf6; leads to nuclear translocation of YB-1 and in consequence to viral replication and cell lysis in vitro and in vivo. Moreover; we show that Xvir03 down-regulates the expression of MDR1 and MRP1; indicating that recruiting YB-1 to the adenoviral E2-la | 16849566 | [
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Inhibition of the multidrug-resistant phenotype by targeting YB-1 with a conditionally oncolytic adenovirus: implications for combinatorial treatment regimen with chemotherapeutic agents. | te promoter for viral replication is responsible for this effect. Thus; nuclear translocation of YB-1 by Xvir03 leads to resensitization of tumor cells to cytotoxic drugs. These data reveal a link between chemotherapy and virotherapy based on the cellular transcription factor YB-1 and provide the basis for formulating a model for a novel combined therapy regimen named Mutually Synergistic Therapy. | 16849566 | [
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Cancers as wounds that do not heal: differences and similarities between renal regeneration/repair and renal cell carcinoma. | Cancers have been described as wounds that do not heal; suggesting that the two share common features. By comparing microarray data from a model of renal regeneration and repair (RRR) with reported gene expression in renal cell carcinoma (RCC); we asked whether those two processes do; in fact; share molecular features and regulatory mechanisms. The majority (77%) of the genes expressed in RRR and RCC were concordantly regulated; whereas only 23% were discordant (i.e.; changed in opposite directions). The or | 16849569 | [
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Cancers as wounds that do not heal: differences and similarities between renal regeneration/repair and renal cell carcinoma. | chestrated processes of regeneration; involving cell proliferation and immune response; were reflected in the concordant genes. The discordant gene signature revealed processes (e.g.; morphogenesis and glycolysis) and pathways (e.g.; hypoxia-inducible factor and insulin-like growth factor-I) that reflect the intrinsic pathologic nature of RCC. This is the first study that compares gene expression patterns in RCC and RRR. It does so; in particular; with relation to the hypothesis that RCC resembles the wound | 16849569 | [
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Cancers as wounds that do not heal: differences and similarities between renal regeneration/repair and renal cell carcinoma. | healing processes seen in RRR. However; careful attention to the genes that are regulated in the discordant direction provides new insights into the critical differences between renal carcinogenesis and wound healing. The observations reported here provide a conceptual framework for further efforts to understand the biology and to develop more effective diagnostic biomarkers and therapeutic strategies for renal tumors and renal ischemia. | 16849569 | [
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Selective antitumor effect of novel protease-mediated photodynamic agent. | A new approach to selective photodynamic therapy (PDT) was developed by designing chlorin e6 (Ce6)-containing macromolecules; which are sensitive to tumor-associated proteases. The agents are nontoxic in their native state but become fluorescent and produce singlet oxygen on protease conversion. Coupled with optimized delivery systems; we show that (a) the agents efficiently accumulate in tumors due to the enhanced permeability and retention effect; (b) the agents are locally activated by proteases; (c) loc | 16849570 | [
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Selective antitumor effect of novel protease-mediated photodynamic agent. | al drug concentrations can be measured by quantitative fluorescence tomography; and (d) light-treated tumors show reduced growth. A single low dose of PDT (0.125 mg Ce6 equivalent/kg) was sufficient to suppress tumor growth by >50%. Activatable singlet oxygen generation agents provide increased efficacy with reduced toxicity; and it could become a powerful PDT. | 16849570 | [
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In vivo tumor targeting using a novel intestinal pathogen-based delivery approach. | Efficient methods for tumor targeting are eagerly awaited and must satisfy several challenges: molecular specificity; transport through physiologic barriers; and capacity to withstand extracellular or intracellular degradation and inactivation by the immune system. Through interaction with its hosts; the intestinal pathogen-produced Shiga toxin has evolved molecular properties that are of interest in this context. Its nontoxic B-subunit binds to the cellular toxin receptor; glycosphingolipid Gb3; which is h | 16849571 | [
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In vivo tumor targeting using a novel intestinal pathogen-based delivery approach. | ighly expressed on human cancers and has recently been reported to be involved in the formation of metastasis in colorectal cancers. Its function as a target for cancer therapy has already been addressed in xenograft experiments. We here show that after oral or i.v. injections in mice; the B-subunit targets spontaneous digestive Gb3-expressing adenocarcinomas. The nontumoral mucosa is devoid of labeling; with the exception of rare enteroendocrine and CD11b-positive cells. As opposed to other delivery tools | 16849571 | [
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In vivo tumor targeting using a novel intestinal pathogen-based delivery approach. | that are often degraded or recycled on cancer cells; the B-subunit stably associates with these cells due to its trafficking via the retrograde transport route. This can be exploited for the in vivo delivery of contrast agents to tumors; as exemplified using fibered confocal fluorescence endoscopy and positron emission tomography (PET) imaging. In conclusion; the data presented in this manuscript lay the groundwork for a novel delivery technology that; in addition to its use for molecular imaging applicatio | 16849571 | [
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In vivo tumor targeting using a novel intestinal pathogen-based delivery approach. | ns such as noninvasive PET; could also be exploited for targeted tumor therapies. | 16849571 | [
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Recombinant human insulin-like growth factor binding protein 3 inhibits growth of human epidermal growth factor receptor-2-overexpressing breast tumors and potentiates herceptin activity in vivo. | Clinical studies indicate that Herceptin (trastuzumab); a recombinant humanized monoclonal antibody directed against the human epidermal growth factor receptor-2 (HER-2) tyrosine kinase growth factor receptor; provides a significant but transient survival advantage to a subset of patients with HER-2-overexpressing metastatic breast cancer when given as a first-line agent. Increased insulin-like growth factor (IGF)-I receptor (IGF-IR) signaling has recently been identified as a potential factor adversely inf | 16849573 | [
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Recombinant human insulin-like growth factor binding protein 3 inhibits growth of human epidermal growth factor receptor-2-overexpressing breast tumors and potentiates herceptin activity in vivo. | luencing the response to Herceptin. We examined the effect of recombinant human IGF binding protein 3 (rhIGFBP-3); an antagonist of IGF-IR signaling; in Herceptin-resistant breast cells in vitro and in tumors in vivo. Consistent with results obtained using HER-2- or IGF-IR-transfected cells (MCF-7/HER2-18 and SKBR3/IGF-IR; respectively); we found that rhIGFBP-3 significantly reduced IGF-I-induced IGF-IR phosphorylation and displayed a synergistic interaction with Herceptin against cultured HER-2-overexpress | 16849573 | [
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Recombinant human insulin-like growth factor binding protein 3 inhibits growth of human epidermal growth factor receptor-2-overexpressing breast tumors and potentiates herceptin activity in vivo. | ing breast cancer cells in vitro. We show; for the first time; the antitumor activity of rhIGFBP-3 against advanced-stage MCF-7/HER2-18-transfected human breast cancer xenografts and its potentiation of Herceptin activity. We also provide evidence that IGF-IR activation counters the early suppressive effect of Herceptin on HER-2 signaling via Akt and p44/p42 mitogen-activated protein kinase (MAPK); and that inhibition of HER-2-overexpressing human breast tumor growth by rhIGFBP-3 is associated with restored | 16849573 | [
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Recombinant human insulin-like growth factor binding protein 3 inhibits growth of human epidermal growth factor receptor-2-overexpressing breast tumors and potentiates herceptin activity in vivo. | down-regulation of Akt and p44/p42 MAPK phosphorylation in vitro and in vivo. These results emphasize the merit of evaluating simultaneous blockade of the HER-2 and IGF-IR pathways using combination therapy with rhIGFBP-3 plus Herceptin in human clinical trials of patients with HER-2-positive breast cancer. | 16849573 | [
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Chronic administration of valproic acid inhibits prostate cancer cell growth in vitro and in vivo. | Valproic acid (VPA) is an established drug in the long-term therapy of seizure disorders. Recently; VPA has been associated with anticancer activity; an effect thought to be mediated through the inhibition of cellular histone deacetylase 1. We investigated the effect of various doses of VPA (0; 1.2; and 5.0 mmol/L) administered either acutely or chronically on histone acetylation; p21 gene expression; androgen receptor expression; prostate-specific antigen (PSA) expression; and cell survival and proliferati | 16849572 | [
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Chronic administration of valproic acid inhibits prostate cancer cell growth in vitro and in vivo. | on in prostate cancer cell lines. We also studied the effect of chronic VPA on tumor xenograft growth in vivo. Our results show that acute treatment (3 days) VPA can increase net histone H3 acetylation and up-regulate p21; AR; and cytosolic PSA expression. Interestingly; the effects on AR and PSA are reversed with chronic treatment. In addition; acute VPA reduces cell survival but has no effect on the subsequent proliferation of surviving cells following drug withdrawal. However; when VPA is chronically adm | 16849572 | [
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Chronic administration of valproic acid inhibits prostate cancer cell growth in vitro and in vivo. | inistered (10-14 days) to prostate cancer cells; even lower doses of VPA result in marked decreases in the net proliferation rate; correlating with increased caspase-2 and caspase-3 activation. These effects are evident in both androgen receptor-positive (LNCaP and C4-2) and androgen receptor-negative (DU145 and PC3) prostate cancer cells. Moreover; chronic VPA treatment results in statistically significant reduction of tumor xenograft growth in vivo. We conclude that acute treatment has nominal effects on | 16849572 | [
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Chronic administration of valproic acid inhibits prostate cancer cell growth in vitro and in vivo. | prostate cancer cell survival and proliferation; but chronic VPA results in profound decreases in proliferation; independently of androgen regulation. | 16849572 | [
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Differential effect of bryostatin 1 and phorbol 12-myristate 13-acetate on HOP-92 cell proliferation is mediated by down-regulation of protein kinase Cdelta. | Bryostatin 1 is currently in clinical trials as a cancer chemotherapeutic agent. Although bryostatin 1; like phorbol 12-myristate 13-acetate (PMA); is a potent activator of protein kinase C (PKC); it induces only a subset of those responses induced by PMA and antagonizes others. We report that; in the HOP-92 non-small cell lung cancer line; bryostatin 1 induced a biphasic proliferative response; with maximal proliferation at 1 to 10 nmol/L. This biphasic response mirrored a biphasic suppression of the level | 16849575 | [
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Differential effect of bryostatin 1 and phorbol 12-myristate 13-acetate on HOP-92 cell proliferation is mediated by down-regulation of protein kinase Cdelta. | of PKCdelta protein; with maximal suppression likewise at 1 to 10 nmol/L bryostatin 1. The typical phorbol ester PMA; in contrast to bryostatin 1; had no effect on the level of PKCdelta and modest suppression of cell proliferation; particularly evident at later treatment times. Flow cytometric analysis revealed changes in the fraction of cells in the G0-G1 and S phases corresponding to the effects on proliferation. Cells overexpressing PKCdelta exhibited a lower rate of cell proliferation compared with con | 16849575 | [
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Differential effect of bryostatin 1 and phorbol 12-myristate 13-acetate on HOP-92 cell proliferation is mediated by down-regulation of protein kinase Cdelta. | trol untreated cells and showed neither a proliferative response nor a loss of PKCdelta in response to bryostatin 1. Conversely; treatment with PKCdelta small interfering RNA significantly increased the cellular growth compared with controls. We conclude that the differential effect on cellular proliferation induced by bryostatin 1 compared with PMA reflects the differential suppression of PKCdelta. | 16849575 | [
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E2F-1 overexpression in U2OS cells increases cyclin B1 levels and cdc2 kinase activity and sensitizes cells to antimitotic agents. | The E2F transcription factors play a critical role in coordinating transcription of specific genes essential for G1-S transition. In early G1; the retinoblastoma protein (pRB) becomes phosphorylated by cyclin-dependent kinases; disrupting pRB binding to E2F-1-3; allowing "free" E2F to regulate genes involved in proliferation. In the present study; we used a tetracycline E2F-1 inducible U2OS osteosarcoma cell line to investigate the effect of increasing levels of E2F-1 on the cytotoxicity of various chemothe | 16849574 | [
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E2F-1 overexpression in U2OS cells increases cyclin B1 levels and cdc2 kinase activity and sensitizes cells to antimitotic agents. | rapeutic drugs. Upon overexpression of E2F-1; there was no detectable change in cytotoxicity to doxorubicin; cisplatin; 5-fluorouracil; or etoposide. In contrast; overexpression of E2F-1 resulted in a marked increase in sensitivity to vinblastine and paclitaxel; drugs that are known to be more effective against cells in M phase. Therefore; we investigated the effect of E2F-1 overexpression on proteins regulating the G2-M transition and M phase; in particular cyclin B1 and cdc2 kinase. Cyclin B1 mRNA and pro | 16849574 | [
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E2F-1 overexpression in U2OS cells increases cyclin B1 levels and cdc2 kinase activity and sensitizes cells to antimitotic agents. | tein levels increased within 24 hours of E2F1 induction together with an increase in associated cdc2 kinase activity. Overexpression of cyclin B1 also resulted in a specific increase in sensitivity to paclitaxel and an increase in the cellular growth rate. Knockdown of cyclin B1 using an RNA interference oligo resulted in a slower cellular growth rate and an increase in resistance to paclitaxel. These studies add support to recent reports that show E2F regulates genes involved in mitotic entry and exit and | 16849574 | [
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E2F-1 overexpression in U2OS cells increases cyclin B1 levels and cdc2 kinase activity and sensitizes cells to antimitotic agents. | allow the suggestion that mitotic inhibitors may have selective effects in tumors that overexpress E2F-1. | 16849574 | [
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Acting via a cell surface receptor, thyroid hormone is a growth factor for glioma cells. | Recent evidence suggests that the thyroid hormone L-thyroxine (T4) stimulates growth of cancer cells via a plasma membrane receptor on integrin alphaVbeta3. The contribution of this recently described receptor for thyroid hormone and receptor-based stimulation of cellular mitogen-activated protein kinase [MAPK; extracellular signal-regulated kinase 1/2 (ERK1/2)] activity; to enhancement of cell proliferation by thyroid hormone was quantitated functionally and by immunologic means in three glioma cell lines | 16849576 | [
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Acting via a cell surface receptor, thyroid hormone is a growth factor for glioma cells. | exposed to T4. At concentrations of 1 to 100 nmol/L; T4 caused proliferation of C6; F98; and GL261 cells; measured by accumulation of proliferating cell nuclear antigen (PCNA) and radiolabeled thymidine incorporation. This effect was inhibited by the T4 analogue; tetraiodothyroacetic acid; and by an alphaVbeta3 RGD recognition site peptide; both of which block T4 binding to integrin alphaVbeta3 but are not agonists. Activation of MAPK by T4 was similarly inhibited by tetraiodothyroacetic acid and the RGD pe | 16849576 | [
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Acting via a cell surface receptor, thyroid hormone is a growth factor for glioma cells. | ptide. The thyroid hormone 3;5;3'-triiodo-L-thyronine (T3) and T4 were equipotent stimulators of PCNA accumulation in C6; F98; and GL261 cells; but physiologic concentrations of T3 are 50-fold lower than those of T4. In conclusion; our studies suggest that glioblastoma cells are thyroid hormone dependent and provide a molecular basis for recent clinical observations that induction of mild hypothyroidism may improve duration of survival in glioblastoma patients. The present experiments infer a novel cell mem | 16849576 | [
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Acting via a cell surface receptor, thyroid hormone is a growth factor for glioma cells. | brane receptor-mediated basis for the growth-promoting activity of thyroid hormone in such tumors and suggest new therapeutic approaches to the treatment of patients with glioblastoma. | 16849576 | [
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Synergy between in situ cryoablation and TLR9 stimulation results in a highly effective in vivo dendritic cell vaccine. | Dendritic cells (DC) are professional antigen-presenting cells that play a pivotal role in the induction of immunity. Ex vivo-generated; tumor antigen-loaded mature DC are currently exploited as cancer vaccines in clinical studies. However; antigen loading and maturation of DC directly in vivo would greatly facilitate the application of DC-based vaccines. We have previously shown that in situ tumor destruction by ablative treatments efficiently delivers antigens for the in vivo induction of antitumor immuni | 16849578 | [
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Synergy between in situ cryoablation and TLR9 stimulation results in a highly effective in vivo dendritic cell vaccine. | ty. In this article; we show that although 20% of the draining lymph node DCs acquire intratumorally injected model antigens after in situ cryoablation; only partial protection against a subsequent tumor rechallenge is observed. However; we also show that a combination treatment of cryoablation plus TLR9 stimulation via CpG-oligodeoxynucleotides is far more effective in the eradication of local and systemic tumors than either treatment modality alone. Analysis of the underlying mechanism revealed that in si | 16849578 | [
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Synergy between in situ cryoablation and TLR9 stimulation results in a highly effective in vivo dendritic cell vaccine. | tu tumor ablation synergizes with TLR9 stimulation to induce DC maturation and efficient cross-presentation in tumor-bearing mice; leading to superior DC function in vivo. Therefore; in situ tumor destruction in combination with CpG-oligodeoxynucleotide administration creates a unique "in situ DC vaccine" that is readily applicable in the clinic. | 16849578 | [
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Combination therapy with anti-CTL antigen-4 and anti-4-1BB antibodies enhances cancer immunity and reduces autoimmunity. | The majority of cancer antigens identified thus far have limited expression in normal tissues. It has been suggested that autoimmune disease is a necessary price for cancer immunity. This notion is supported by a recent clinical trial involving an anti-CTL antigen-4 (CTLA-4) antibody that showed significant clinical responses but severe autoimmune diseases in melanoma patients. To selectively modulate cancer immunity and autoimmunity; we used anti-CTLA-4 and anti-4-1BB antibodies to treat mice with a preexi | 16849577 | [
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Combination therapy with anti-CTL antigen-4 and anti-4-1BB antibodies enhances cancer immunity and reduces autoimmunity. | sting cancer; MC38. The combination of the two antibodies led to CD8 T-cell-mediated rejection of large established MC38 tumors and long-lasting immunity to the same tumor cells; although the same regimen was not effective for B16 melanoma. More importantly; whereas individual antibodies induced inflammation and autoimmune manifestations; combination therapy increased cancer immunity while reducing autoimmunity. The reduction of autoimmune effects correlates with an increased function of regulatory T cells. | 16849577 | [
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Combination therapy with anti-CTL antigen-4 and anti-4-1BB antibodies enhances cancer immunity and reduces autoimmunity. | Our results suggest a novel approach to simultaneously enhance cancer immunity and reduce autoimmunity. | 16849577 | [
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Cancer immunotherapy by interleukin-21: potential treatment strategies evaluated in a mathematical model. | The newly characterized interleukin (IL)-21 plays a central role in the transition from innate immunity to adaptive immunity and shows substantial tumor regression in mice. IL-21 is now developed as a cancer immunotherapeutic drug; but conditions for efficacious therapy; and the conflicting immunostimulatory and immunoinhibitory influence of the cytokine; are yet to be defined. We studied the effects of IL-21 on tumor eradication in a mathematical model focusing on natural killer (NK) cell-mediated and CD8+ | 16849579 | [
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Cancer immunotherapy by interleukin-21: potential treatment strategies evaluated in a mathematical model. | T-cell-mediated lysis of tumor cells. Model parameters were estimated using results in tumor-bearing mice treated with IL-21 via cytokine gene therapy (CGT); hydrodynamics-based gene delivery (HGD); or standard interval dosing (SID). Our model accurately retrieved experimental growth dynamics in the nonimmunogenic B16 melanoma and the immunogenic MethA and MCA205 fibrosarcomas; showing a strong dependence of the NK-cell/CD8+ T-cell balance on tumor immunogenicity. Moreover; in melanoma; simulations of CGT- | 16849579 | [
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Cancer immunotherapy by interleukin-21: potential treatment strategies evaluated in a mathematical model. | like dosing regimens; dynamically determined according to tumor mass changes; resulted in efficient disease elimination. In contrast; in fibrosarcoma; such a strategy was not superior to that of fixed dosing regimens; HGD or SID. Our model supports clinical use of IL-21 as a potent stimulator of cellular immunity against cancer; and suggests selecting the immunotherapy strategy according to tumor immunogenicity. Nonimmunogenic tumors; but not highly immunogenic tumors; should be controlled by IL-21 dosing; | 16849579 | [
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Cancer immunotherapy by interleukin-21: potential treatment strategies evaluated in a mathematical model. | which depends on tumor mass at the time of administration. This method imitates; yet amplifies; the natural anticancer immune response rather than accelerates only one of the response arms in an unbalanced manner. | 16849579 | [
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Comparative analysis of regulatory and effector T cells in progressively growing versus rejecting tumors of similar origins. | Although regulatory T cells (Tregs) have been detected in clinically apparent and experimentally induced tumors; the significance of their presence is obscured because past studies examined late-stage tumors that had formed in immunocompetent hosts and thus had evolved mechanisms to escape immunologic recognition and/or elimination. Herein; we report the first comparative analysis of the antitumor response to 3'-methylcholanthrene-induced tumors; which either grow progressively (progressor tumors) or are re | 16849580 | [
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Comparative analysis of regulatory and effector T cells in progressively growing versus rejecting tumors of similar origins. | jected by the immune system (regressor tumors). Surprisingly; we found that both progressor and regressor tumors harbored proliferating (i.e.; activated) Foxp3+CD25+Tregs. However; progressor tumors contained a higher percentage of Tregs in the lymphocyte subset versus regressor tumors. The Tregs in progressor tumors were derived from peripheral CD25+ natural Tregs; accumulated early after tumor challenge and were actively proliferating; suggesting that progressor tumors recruited and/or activated endogenou | 16849580 | [
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Comparative analysis of regulatory and effector T cells in progressively growing versus rejecting tumors of similar origins. | s Tregs as a mechanism of escaping immune destruction. To explore whether Tregs directly contributed to the progressive growth phenotype of progressor tumors; we monitored tumor outgrowth in naive wild-type recipients pretreated with either a control monoclonal antibody (mAb) or a depleting CD25-specific mAb. In mice predepleted of CD25+ cells; the tumors that subsequently developed displayed an increased accumulation of proliferating CD8+ T cells and were rejected. These results show that; although Tregs a | 16849580 | [
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Comparative analysis of regulatory and effector T cells in progressively growing versus rejecting tumors of similar origins. | re activated in both regressor and progressor tumors; the ratio of regulatory to effector T cells is critical in determining whether the host successfully rejects the tumor or eventually succumbs to tumor outgrowth. | 16849580 | [
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Single-cell cloning of human, donor-derived antileukemia T-cell lines for in vitro separation of graft-versus-leukemia effect from graft-versus-host reaction. | In previous studies; we showed the possibility of expanding in vitro polyclonal CTL lines directed against patient leukemia cells using effector cells derived from both HLA-matched and HLA-mismatched hematopoietic stem cell donors. Some CTL lines; especially those derived from an HLA-disparate donor; displayed residual alloreactivity against patient nonmalignant cells. In this study; we evaluated the possibility of separating in vitro CTLs with selective graft-versus-leukemia (GVL) activity from those poten | 16849581 | [
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Single-cell cloning of human, donor-derived antileukemia T-cell lines for in vitro separation of graft-versus-leukemia effect from graft-versus-host reaction. | tially involved in the development of graft-versus-host disease (GVHD) through single T-cell cloning of antileukemia polyclonal CTL lines. We showed that CTLs that were expanded from a single T-cell clone (TCC); able to selectively kill leukemia blasts and devoid of alloreactivity towards nonmalignant cells; can be obtained from antileukemia alloreactive polyclonal CTL lines. TCCs expressed a wide repertoire of different T-cell receptor (TCR)-Vbeta families; mainly produced IFNgamma and interleukin 2; irres | 16849581 | [
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Single-cell cloning of human, donor-derived antileukemia T-cell lines for in vitro separation of graft-versus-leukemia effect from graft-versus-host reaction. | pective of CD8 or CD4 phenotype; and could be extensively expanded in vitro without losing their peculiar functional features. The feasibility of our approach for in vitro separation of GVL from GVH reaction opens perspectives for using TCCs; which are selectively reactive towards leukemia blasts; for antileukemia adoptive immune therapy approaches after hematopoietic stem cell transplantation; in particular from HLA-mismatched donors. | 16849581 | [
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Bortezomib and depsipeptide sensitize tumors to tumor necrosis factor-related apoptosis-inducing ligand: a novel method to potentiate natural killer cell tumor cytotoxicity. | The proteasome inhibitor; bortezomib; and the histone deacetylase inhibitor; depsipeptide (FK228); up-regulate tumor death receptors. Therefore; we investigated whether pretreatment of malignant cells with these agents would potentiate natural killer (NK)-mediated tumor killing. NK cells isolated from healthy donors and patients with cancer were expanded in vitro and then tested for cytotoxicity against tumor cell lines before and after exposure to bortezomib or depsipeptide. In 11 of 13 (85%) renal cell ca | 16849582 | [
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Bortezomib and depsipeptide sensitize tumors to tumor necrosis factor-related apoptosis-inducing ligand: a novel method to potentiate natural killer cell tumor cytotoxicity. | rcinoma cell lines and in 16 of 37 (43%) other cancer cell lines; exposure to these drugs significantly increased NK cell-mediated tumor lysis compared with untreated tumor controls (P < 0.001). Furthermore; NK cells expanded from patients with metastatic renal cell carcinoma were significantly more cytotoxic against autologous tumor cells when pretreated with either bortezomib or depsipeptide compared with untreated tumors. Tumors sensitized to NK cell cytotoxicity showed a significant increase in surface | 16849582 | [
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Bortezomib and depsipeptide sensitize tumors to tumor necrosis factor-related apoptosis-inducing ligand: a novel method to potentiate natural killer cell tumor cytotoxicity. | expression of DR5 [tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-R2; P < 0.05]; in contrast; surface expression of MHC class I; MIC-A/B; DR4 (TRAIL-R1); and Fas (CD95) did not change. The enhanced susceptibility to NK cell killing was completely abolished by blocking TRAIL on NK cells; and partially abolished by blocking DR5 on tumor cells. These findings show that drug-induced sensitization to TRAIL could be used as a novel strategy to potentiate the anticancer effects of adoptively infus | 16849582 | [
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Bortezomib and depsipeptide sensitize tumors to tumor necrosis factor-related apoptosis-inducing ligand: a novel method to potentiate natural killer cell tumor cytotoxicity. | ed NK cells in patients with cancer. | 16849582 | [
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Hic-5/ARA55, a LIM domain-containing nuclear receptor coactivator expressed in prostate stromal cells. | Prostate gland development and growth requires both androgen action and epithelial-stromal communications. In fact; androgen signaling through the androgen receptor (AR) may be important in both stromal and epithelial cells of the prostate. Because interaction of AR with the coactivator; Hic-5/ARA55; results in enhanced androgen-induced transcription; we analyzed Hic-5/ARA55 expression in prostate tissue sections from normal human donors and prostate cancer patients. In each sample; Hic-5/ARA55 expression w | 16849583 | [
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Hic-5/ARA55, a LIM domain-containing nuclear receptor coactivator expressed in prostate stromal cells. | as confined to the stromal compartment of the prostate. Furthermore; a prostate stromal cell line; WPMY-1 cells; expresses Hic-5/ARA55; which is localized both at focal adhesion complexes and within the soluble cytoplasmic compartment. The ability of Hic-5/ARA55 to shuttle between the nuclear and cytoplasmic compartments was revealed on inhibition of nuclear export with leptomycin B. Small interfering RNA ablation experiments established endogenous Hic-5/ARA55 as a coactivator for both viral and endogenous | 16849583 | [
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Hic-5/ARA55, a LIM domain-containing nuclear receptor coactivator expressed in prostate stromal cells. | cellular AR-regulated genes. Finally; the mechanism of Hic-5/ARA55 coactivator activity in WPMY-1 cells was revealed by chromatin immunoprecipitation analysis that showed its androgen-dependent recruitment to the promoter of the stromal androgen-responsive keratinocyte growth factor gene. These data provide the first demonstration of a stromal-specific AR coactivator that has an effect on an androgen-regulated growth factor that is essential for stromal/epithelial cell communication in the prostate. | 16849583 | [
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