Epidermal growth factor induces bladder cancer cell proliferation through activation of the androgen receptor
Androgen receptor (AR) signals have been suggested to contribute to bladder tumorigenesis and cancer progression. Activation of epidermal growth factor receptor (EGFR) also leads to stimulation of bladder tumor growth. However, crosstalk between AR and EGFR pathways in bladder cancer remains unchara...
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| Veröffentlicht in: | International journal of oncology 2012-11, Vol.41 (5), p.1587-1592 |
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| creator | IZUMI, KOJI ZHENG, YICHUN LI, YI ZAENGLE, JACQUELINE MIYAMOTO, HIROSHI |
| description | Androgen receptor (AR) signals have been suggested to contribute to bladder tumorigenesis and cancer progression. Activation of epidermal growth factor receptor (EGFR) also leads to stimulation of bladder tumor growth. However, crosstalk between AR and EGFR pathways in bladder cancer remains uncharacterized. We have recently shown that androgens activate the EGFR pathway in bladder cancer cells. The purpose of this study was to investigate the effects of EGF on AR activity in bladder cancer. EGF increased AR transcriptional activity by 1.2-, 1.9- and 2.0-fold in UMUC3, 5637-AR and J82-AR cell lines, respectively, over mock treatment and a specific EGFR inhibitor, PD168393, antagonized the EGF effect. Combined treatment of EGF and dihydrotestosterone (DHT) further induced AR transactivation while an AR antagonist, hydroxyflutamide (HF), abolished the effect of not only DHT but also EGF. In growth assays, EGF alone/DHT alone/EGF+DHT increased cell numbers by 16/12/19%, 6/14/18% and 30/12/38% in UMUC3-control-shRNA, 5637-AR and J82-AR, respectively, whereas the effects of EGF were marginal or less significant in UMUC3-AR-shRNA (8%) or AR-negative 5637-V ( |
| doi_str_mv | 10.3892/ijo.2012.1593 |
| format | Article |
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Activation of epidermal growth factor receptor (EGFR) also leads to stimulation of bladder tumor growth. However, crosstalk between AR and EGFR pathways in bladder cancer remains uncharacterized. We have recently shown that androgens activate the EGFR pathway in bladder cancer cells. The purpose of this study was to investigate the effects of EGF on AR activity in bladder cancer. EGF increased AR transcriptional activity by 1.2-, 1.9- and 2.0-fold in UMUC3, 5637-AR and J82-AR cell lines, respectively, over mock treatment and a specific EGFR inhibitor, PD168393, antagonized the EGF effect. Combined treatment of EGF and dihydrotestosterone (DHT) further induced AR transactivation while an AR antagonist, hydroxyflutamide (HF), abolished the effect of not only DHT but also EGF. In growth assays, EGF alone/DHT alone/EGF+DHT increased cell numbers by 16/12/19%, 6/14/18% and 30/12/38% in UMUC3-control-shRNA, 5637-AR and J82-AR, respectively, whereas the effects of EGF were marginal or less significant in UMUC3-AR-shRNA (8%) or AR-negative 5637-V (<1%) and J82-V (17%) cells. HF treatment at least partially counteracted the EGF effect on the growth of AR-positive cells. Western blotting demonstrated that EGF, especially in the presence of DHT, upregulated the expression of the p160 coactivator TIF2 and HF again blocked this stimulation. Co-immunoprecipitation revealed the association between AR and estrogen receptor (ER)-β or Src in UMUC3 cells and stronger associations with EGF treatment, implying the involvement of the AR/ER/Src complex in EGF-increased AR transactivation and cell growth. Current results, thus, suggest that EGF promotes bladder cancer cell proliferation via modulation of AR signals. Taken together with our previous findings, crosstalk between EGFR and AR pathways can play an important role in the progression of bladder cancer.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.2012.1593</identifier><identifier>PMID: 22922989</identifier><language>eng</language><publisher>Athens: D.A. Spandidos</publisher><subject>androgen receptor ; Androgen Receptor Antagonists - pharmacology ; Androgens ; Biological and medical sciences ; Biotechnology ; Bladder cancer ; Cell growth ; Cell Line, Tumor ; Cell Proliferation - drug effects ; Charcoal ; Cloning ; Epidermal growth factor ; Epidermal Growth Factor - pharmacology ; Gene expression ; Gene Expression Regulation, Neoplastic - drug effects ; Humans ; hydroxyflutamide ; Ligands ; Medical sciences ; Nephrology. Urinary tract diseases ; Nuclear Receptor Coactivator 2 - genetics ; Nuclear Receptor Coactivator 2 - metabolism ; Phosphorylation ; Plasmids ; Prostate cancer ; Protein Binding ; Proteins ; Receptor, Epidermal Growth Factor - metabolism ; Receptors, Androgen - genetics ; Receptors, Androgen - metabolism ; Receptors, Estrogen - metabolism ; Signal Transduction - drug effects ; Src ; src-Family Kinases - metabolism ; Transcriptional Activation ; transcriptional intermediary factor 2 ; Tumors ; Tumors of the urinary system ; Urinary Bladder Neoplasms - genetics ; Urinary Bladder Neoplasms - metabolism ; Urinary tract. Prostate gland</subject><ispartof>International journal of oncology, 2012-11, Vol.41 (5), p.1587-1592</ispartof><rights>Copyright © 2012, Spandidos Publications</rights><rights>2015 INIST-CNRS</rights><rights>Copyright Spandidos Publications UK Ltd. 2012</rights><rights>Copyright © 2012, Spandidos Publications 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c543t-848571803e35ffa6324d6e6b549b1122adfedc7065f8b80866608153ae5641513</citedby><cites>FETCH-LOGICAL-c543t-848571803e35ffa6324d6e6b549b1122adfedc7065f8b80866608153ae5641513</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,5556,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=26430300$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22922989$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>IZUMI, KOJI</creatorcontrib><creatorcontrib>ZHENG, YICHUN</creatorcontrib><creatorcontrib>LI, YI</creatorcontrib><creatorcontrib>ZAENGLE, JACQUELINE</creatorcontrib><creatorcontrib>MIYAMOTO, HIROSHI</creatorcontrib><title>Epidermal growth factor induces bladder cancer cell proliferation through activation of the androgen receptor</title><title>International journal of oncology</title><addtitle>Int J Oncol</addtitle><description>Androgen receptor (AR) signals have been suggested to contribute to bladder tumorigenesis and cancer progression. Activation of epidermal growth factor receptor (EGFR) also leads to stimulation of bladder tumor growth. However, crosstalk between AR and EGFR pathways in bladder cancer remains uncharacterized. We have recently shown that androgens activate the EGFR pathway in bladder cancer cells. The purpose of this study was to investigate the effects of EGF on AR activity in bladder cancer. EGF increased AR transcriptional activity by 1.2-, 1.9- and 2.0-fold in UMUC3, 5637-AR and J82-AR cell lines, respectively, over mock treatment and a specific EGFR inhibitor, PD168393, antagonized the EGF effect. Combined treatment of EGF and dihydrotestosterone (DHT) further induced AR transactivation while an AR antagonist, hydroxyflutamide (HF), abolished the effect of not only DHT but also EGF. In growth assays, EGF alone/DHT alone/EGF+DHT increased cell numbers by 16/12/19%, 6/14/18% and 30/12/38% in UMUC3-control-shRNA, 5637-AR and J82-AR, respectively, whereas the effects of EGF were marginal or less significant in UMUC3-AR-shRNA (8%) or AR-negative 5637-V (<1%) and J82-V (17%) cells. HF treatment at least partially counteracted the EGF effect on the growth of AR-positive cells. Western blotting demonstrated that EGF, especially in the presence of DHT, upregulated the expression of the p160 coactivator TIF2 and HF again blocked this stimulation. Co-immunoprecipitation revealed the association between AR and estrogen receptor (ER)-β or Src in UMUC3 cells and stronger associations with EGF treatment, implying the involvement of the AR/ER/Src complex in EGF-increased AR transactivation and cell growth. Current results, thus, suggest that EGF promotes bladder cancer cell proliferation via modulation of AR signals. Taken together with our previous findings, crosstalk between EGFR and AR pathways can play an important role in the progression of bladder cancer.</description><subject>androgen receptor</subject><subject>Androgen Receptor Antagonists - pharmacology</subject><subject>Androgens</subject><subject>Biological and medical sciences</subject><subject>Biotechnology</subject><subject>Bladder cancer</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation - drug effects</subject><subject>Charcoal</subject><subject>Cloning</subject><subject>Epidermal growth factor</subject><subject>Epidermal Growth Factor - pharmacology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation, Neoplastic - drug effects</subject><subject>Humans</subject><subject>hydroxyflutamide</subject><subject>Ligands</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nuclear Receptor Coactivator 2 - genetics</subject><subject>Nuclear Receptor Coactivator 2 - metabolism</subject><subject>Phosphorylation</subject><subject>Plasmids</subject><subject>Prostate cancer</subject><subject>Protein Binding</subject><subject>Proteins</subject><subject>Receptor, Epidermal Growth Factor - metabolism</subject><subject>Receptors, Androgen - genetics</subject><subject>Receptors, Androgen - metabolism</subject><subject>Receptors, Estrogen - metabolism</subject><subject>Signal Transduction - drug effects</subject><subject>Src</subject><subject>src-Family Kinases - metabolism</subject><subject>Transcriptional Activation</subject><subject>transcriptional intermediary factor 2</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary Bladder Neoplasms - genetics</subject><subject>Urinary Bladder Neoplasms - metabolism</subject><subject>Urinary tract. Prostate gland</subject><issn>1019-6439</issn><issn>1791-2423</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNpVkU2LFDEQhoMo7rp69CoBEU8Z8z3JRViW9QMWvOg5pNPJTIaeTpt0r_jvrWbGXQ2BCpWn3irqReg1oxthLP-QD2XDKeMbpqx4gi7Z1jLCJRdP4U2ZJVoKe4FetHaglCtF2XN0wbmFa-wlOt5OuY_16Ae8q-XXvMfJh7lUnMd-CbHhbvA9ADj4MawhDgOeahlyitXPuYx43tey7PYY6vL9KVUSZCP2Y1_LLo64xhAnUH2JniU_tPjqHK_Qj0-332--kLtvn7_eXN-RoKSYiZFGbZmhIgqVkteCy15H3SlpO8Y4932KfdhSrZLpDDVaa2qYEj4qLZli4gp9POlOS3cENI5z9YObaj76-tsVn93_P2Peu125d0IZoSUFgbdngVp-LrHN7lCWOsLMjlnBBYezUuREhVpaqzE9dGDUre44cMet7rjVHeDf_DvWA_3XDgDenQHfgh9ShaXn9siBl1TQtfH7E9cm2HHuyyMDHYlkhCrClNmKP_GZprg</recordid><startdate>20121101</startdate><enddate>20121101</enddate><creator>IZUMI, KOJI</creator><creator>ZHENG, YICHUN</creator><creator>LI, YI</creator><creator>ZAENGLE, JACQUELINE</creator><creator>MIYAMOTO, HIROSHI</creator><general>D.A. Spandidos</general><general>Editorial Academy of the International Journal of Oncology</general><general>Spandidos Publications UK Ltd</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>5PM</scope></search><sort><creationdate>20121101</creationdate><title>Epidermal growth factor induces bladder cancer cell proliferation through activation of the androgen receptor</title><author>IZUMI, KOJI ; ZHENG, YICHUN ; LI, YI ; ZAENGLE, JACQUELINE ; MIYAMOTO, HIROSHI</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c543t-848571803e35ffa6324d6e6b549b1122adfedc7065f8b80866608153ae5641513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>androgen receptor</topic><topic>Androgen Receptor Antagonists - pharmacology</topic><topic>Androgens</topic><topic>Biological and medical sciences</topic><topic>Biotechnology</topic><topic>Bladder cancer</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation - drug effects</topic><topic>Charcoal</topic><topic>Cloning</topic><topic>Epidermal growth factor</topic><topic>Epidermal Growth Factor - pharmacology</topic><topic>Gene expression</topic><topic>Gene Expression Regulation, Neoplastic - drug effects</topic><topic>Humans</topic><topic>hydroxyflutamide</topic><topic>Ligands</topic><topic>Medical sciences</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nuclear Receptor Coactivator 2 - genetics</topic><topic>Nuclear Receptor Coactivator 2 - metabolism</topic><topic>Phosphorylation</topic><topic>Plasmids</topic><topic>Prostate cancer</topic><topic>Protein Binding</topic><topic>Proteins</topic><topic>Receptor, Epidermal Growth Factor - metabolism</topic><topic>Receptors, Androgen - genetics</topic><topic>Receptors, Androgen - metabolism</topic><topic>Receptors, Estrogen - metabolism</topic><topic>Signal Transduction - drug effects</topic><topic>Src</topic><topic>src-Family Kinases - metabolism</topic><topic>Transcriptional Activation</topic><topic>transcriptional intermediary factor 2</topic><topic>Tumors</topic><topic>Tumors of the urinary system</topic><topic>Urinary Bladder Neoplasms - genetics</topic><topic>Urinary Bladder Neoplasms - metabolism</topic><topic>Urinary tract. 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Activation of epidermal growth factor receptor (EGFR) also leads to stimulation of bladder tumor growth. However, crosstalk between AR and EGFR pathways in bladder cancer remains uncharacterized. We have recently shown that androgens activate the EGFR pathway in bladder cancer cells. The purpose of this study was to investigate the effects of EGF on AR activity in bladder cancer. EGF increased AR transcriptional activity by 1.2-, 1.9- and 2.0-fold in UMUC3, 5637-AR and J82-AR cell lines, respectively, over mock treatment and a specific EGFR inhibitor, PD168393, antagonized the EGF effect. Combined treatment of EGF and dihydrotestosterone (DHT) further induced AR transactivation while an AR antagonist, hydroxyflutamide (HF), abolished the effect of not only DHT but also EGF. In growth assays, EGF alone/DHT alone/EGF+DHT increased cell numbers by 16/12/19%, 6/14/18% and 30/12/38% in UMUC3-control-shRNA, 5637-AR and J82-AR, respectively, whereas the effects of EGF were marginal or less significant in UMUC3-AR-shRNA (8%) or AR-negative 5637-V (<1%) and J82-V (17%) cells. HF treatment at least partially counteracted the EGF effect on the growth of AR-positive cells. Western blotting demonstrated that EGF, especially in the presence of DHT, upregulated the expression of the p160 coactivator TIF2 and HF again blocked this stimulation. Co-immunoprecipitation revealed the association between AR and estrogen receptor (ER)-β or Src in UMUC3 cells and stronger associations with EGF treatment, implying the involvement of the AR/ER/Src complex in EGF-increased AR transactivation and cell growth. Current results, thus, suggest that EGF promotes bladder cancer cell proliferation via modulation of AR signals. Taken together with our previous findings, crosstalk between EGFR and AR pathways can play an important role in the progression of bladder cancer.</abstract><cop>Athens</cop><pub>D.A. Spandidos</pub><pmid>22922989</pmid><doi>10.3892/ijo.2012.1593</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1019-6439 |
| ispartof | International journal of oncology, 2012-11, Vol.41 (5), p.1587-1592 |
| issn | 1019-6439 1791-2423 |
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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | androgen receptor Androgen Receptor Antagonists - pharmacology Androgens Biological and medical sciences Biotechnology Bladder cancer Cell growth Cell Line, Tumor Cell Proliferation - drug effects Charcoal Cloning Epidermal growth factor Epidermal Growth Factor - pharmacology Gene expression Gene Expression Regulation, Neoplastic - drug effects Humans hydroxyflutamide Ligands Medical sciences Nephrology. Urinary tract diseases Nuclear Receptor Coactivator 2 - genetics Nuclear Receptor Coactivator 2 - metabolism Phosphorylation Plasmids Prostate cancer Protein Binding Proteins Receptor, Epidermal Growth Factor - metabolism Receptors, Androgen - genetics Receptors, Androgen - metabolism Receptors, Estrogen - metabolism Signal Transduction - drug effects Src src-Family Kinases - metabolism Transcriptional Activation transcriptional intermediary factor 2 Tumors Tumors of the urinary system Urinary Bladder Neoplasms - genetics Urinary Bladder Neoplasms - metabolism Urinary tract. Prostate gland |
| title | Epidermal growth factor induces bladder cancer cell proliferation through activation of the androgen receptor |
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