ErbB-2 signaling is involved in regulating PSA secretion in androgen-independent human prostate cancer LNCaP C-81 cells
The expression and secretion of prostate-specific antigen (PSA) are regulated by androgens in normal prostate secretory epithelial cells. In prostate cancer patients, the serum PSA level is usually elevated and cancer cells are initially responsive to androgens. However, those cancer cells become an...
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| Veröffentlicht in: | Oncogene 2003-02, Vol.22 (5), p.781-796 |
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| creator | Lee, Ming-Shyue Igawa, Tsukasa Yuan, Ta-Chun Zhang, Xiu-Qing Lin, Fen-Fen Lin, Ming-Fong |
| description | The expression and secretion of prostate-specific antigen (PSA) are regulated by androgens in normal prostate secretory epithelial cells. In prostate cancer patients, the serum PSA level is usually elevated and cancer cells are initially responsive to androgens. However, those cancer cells become androgen-independent after androgen ablation therapy. In hormone-refractory cancer patients, even in an androgen-deprived environment, the circulation level of PSA rebounds and is constitutively elevated through a yet unknown mechanism. Tyrosine phosphorylation of ErbB-2 is involved in regulating the androgen-responsive phenotype of prostate cancer cells, and it is at least partly regulated by the cellular form of prostatic acid phosphatase (PAcP), a prostate-unique protein tyrosine phosphatase. We investigated the ErbB-2 signal pathway in androgen-independent PSA secretion. LNCaP C-81 cells, which are androgen-independent LNCaP cells lacking endogenous PAcP expression with a hypertyrosine phosphorylated ErbB-2, secreted a higher level of PSA in conditioned media than did androgen-sensitive LNCaP C-33 parental cells. A restored expression of cellular PAcP in C-81 cells was concurrent with a decrease in tyrophosphorylation of ErbB-2 and reduction of PSA secretion. Moreover, transient transfection of C-33 cells with the wild-type ErbB-2 or a constitutively active mutant of MEK1 cDNA resulted in an increased level of secreted PSA. The elevation of secreted PSA level by the forced expression of ErbB-2 was inhibited by an MEK inhibitor, PD98059. In C-81 cells, the expression of a dominant negative mutant of ErbB-2 reduced the secreted level of PSA. The inhibition of ErbB-2 or mitogen-activated protein (MAP) kinases by specific inhibitors AG879, AG825, or PD98059 led to a decrease in PSA secretion. Taken together, our data clearly indicate that the ErbB-2 signal pathway via MAP kinases (ERK1/2) is involved in regulating the secretion of PSA by androgen-independent human prostate cancer LNCaP C-81 cells in an androgen-depleted environment. |
| doi_str_mv | 10.1038/sj.onc.1206066 |
| format | Article |
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In prostate cancer patients, the serum PSA level is usually elevated and cancer cells are initially responsive to androgens. However, those cancer cells become androgen-independent after androgen ablation therapy. In hormone-refractory cancer patients, even in an androgen-deprived environment, the circulation level of PSA rebounds and is constitutively elevated through a yet unknown mechanism. Tyrosine phosphorylation of ErbB-2 is involved in regulating the androgen-responsive phenotype of prostate cancer cells, and it is at least partly regulated by the cellular form of prostatic acid phosphatase (PAcP), a prostate-unique protein tyrosine phosphatase. We investigated the ErbB-2 signal pathway in androgen-independent PSA secretion. LNCaP C-81 cells, which are androgen-independent LNCaP cells lacking endogenous PAcP expression with a hypertyrosine phosphorylated ErbB-2, secreted a higher level of PSA in conditioned media than did androgen-sensitive LNCaP C-33 parental cells. A restored expression of cellular PAcP in C-81 cells was concurrent with a decrease in tyrophosphorylation of ErbB-2 and reduction of PSA secretion. Moreover, transient transfection of C-33 cells with the wild-type ErbB-2 or a constitutively active mutant of MEK1 cDNA resulted in an increased level of secreted PSA. The elevation of secreted PSA level by the forced expression of ErbB-2 was inhibited by an MEK inhibitor, PD98059. In C-81 cells, the expression of a dominant negative mutant of ErbB-2 reduced the secreted level of PSA. The inhibition of ErbB-2 or mitogen-activated protein (MAP) kinases by specific inhibitors AG879, AG825, or PD98059 led to a decrease in PSA secretion. Taken together, our data clearly indicate that the ErbB-2 signal pathway via MAP kinases (ERK1/2) is involved in regulating the secretion of PSA by androgen-independent human prostate cancer LNCaP C-81 cells in an androgen-depleted environment.</description><identifier>ISSN: 0950-9232</identifier><identifier>EISSN: 1476-5594</identifier><identifier>DOI: 10.1038/sj.onc.1206066</identifier><identifier>PMID: 12569372</identifier><identifier>CODEN: ONCNES</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Ablation ; Acid Phosphatase ; Androgens ; Androgens - physiology ; Antigens ; Apoptosis ; Biochemistry ; Biological and medical sciences ; Cell Biology ; Cell Division - physiology ; Cell physiology ; Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes ; Classical genetics, quantitative genetics, hybrids ; Culture Media, Conditioned - metabolism ; Fundamental and applied biological sciences. Psychology ; Genetics of eukaryotes. Biological and molecular evolution ; Genotype & phenotype ; Human ; Human Genetics ; Humans ; Internal Medicine ; Kinases ; Male ; MAP Kinase Kinase Kinase 1 ; Medicine ; Medicine & Public Health ; Mitogen-Activated Protein Kinases - physiology ; Molecular and cellular biology ; Molecular biology ; oncogenomics ; Oncology ; Phosphatase ; Prostate cancer ; Prostate-Specific Antigen - metabolism ; Prostate-Specific Antigen - secretion ; Prostatic Neoplasms ; Protein Tyrosine Phosphatases - physiology ; Protein-Serine-Threonine Kinases - antagonists & inhibitors ; Proteins ; Receptor, ErbB-2 - antagonists & inhibitors ; Receptor, ErbB-2 - physiology ; Signal transduction ; Signal Transduction - physiology ; Tumor Cells, Cultured ; Up-Regulation - physiology</subject><ispartof>Oncogene, 2003-02, Vol.22 (5), p.781-796</ispartof><rights>Springer Nature Limited 2003</rights><rights>2003 INIST-CNRS</rights><rights>COPYRIGHT 2003 Nature Publishing Group</rights><rights>Copyright Nature Publishing Group Feb 6, 2003</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c486t-532b5e1c2ad44ec0d917687538e7b08b6616beea74c8317143d2a82ec5fdef873</citedby><cites>FETCH-LOGICAL-c486t-532b5e1c2ad44ec0d917687538e7b08b6616beea74c8317143d2a82ec5fdef873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1038/sj.onc.1206066$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1038/sj.onc.1206066$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14680620$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12569372$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lee, Ming-Shyue</creatorcontrib><creatorcontrib>Igawa, Tsukasa</creatorcontrib><creatorcontrib>Yuan, Ta-Chun</creatorcontrib><creatorcontrib>Zhang, Xiu-Qing</creatorcontrib><creatorcontrib>Lin, Fen-Fen</creatorcontrib><creatorcontrib>Lin, Ming-Fong</creatorcontrib><title>ErbB-2 signaling is involved in regulating PSA secretion in androgen-independent human prostate cancer LNCaP C-81 cells</title><title>Oncogene</title><addtitle>Oncogene</addtitle><addtitle>Oncogene</addtitle><description>The expression and secretion of prostate-specific antigen (PSA) are regulated by androgens in normal prostate secretory epithelial cells. In prostate cancer patients, the serum PSA level is usually elevated and cancer cells are initially responsive to androgens. However, those cancer cells become androgen-independent after androgen ablation therapy. In hormone-refractory cancer patients, even in an androgen-deprived environment, the circulation level of PSA rebounds and is constitutively elevated through a yet unknown mechanism. Tyrosine phosphorylation of ErbB-2 is involved in regulating the androgen-responsive phenotype of prostate cancer cells, and it is at least partly regulated by the cellular form of prostatic acid phosphatase (PAcP), a prostate-unique protein tyrosine phosphatase. We investigated the ErbB-2 signal pathway in androgen-independent PSA secretion. LNCaP C-81 cells, which are androgen-independent LNCaP cells lacking endogenous PAcP expression with a hypertyrosine phosphorylated ErbB-2, secreted a higher level of PSA in conditioned media than did androgen-sensitive LNCaP C-33 parental cells. A restored expression of cellular PAcP in C-81 cells was concurrent with a decrease in tyrophosphorylation of ErbB-2 and reduction of PSA secretion. Moreover, transient transfection of C-33 cells with the wild-type ErbB-2 or a constitutively active mutant of MEK1 cDNA resulted in an increased level of secreted PSA. The elevation of secreted PSA level by the forced expression of ErbB-2 was inhibited by an MEK inhibitor, PD98059. In C-81 cells, the expression of a dominant negative mutant of ErbB-2 reduced the secreted level of PSA. The inhibition of ErbB-2 or mitogen-activated protein (MAP) kinases by specific inhibitors AG879, AG825, or PD98059 led to a decrease in PSA secretion. Taken together, our data clearly indicate that the ErbB-2 signal pathway via MAP kinases (ERK1/2) is involved in regulating the secretion of PSA by androgen-independent human prostate cancer LNCaP C-81 cells in an androgen-depleted environment.</description><subject>Ablation</subject><subject>Acid Phosphatase</subject><subject>Androgens</subject><subject>Androgens - physiology</subject><subject>Antigens</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biological and medical sciences</subject><subject>Cell Biology</subject><subject>Cell Division - physiology</subject><subject>Cell physiology</subject><subject>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</subject><subject>Classical genetics, quantitative genetics, hybrids</subject><subject>Culture Media, Conditioned - metabolism</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Genetics of eukaryotes. Biological and molecular evolution</subject><subject>Genotype & phenotype</subject><subject>Human</subject><subject>Human Genetics</subject><subject>Humans</subject><subject>Internal Medicine</subject><subject>Kinases</subject><subject>Male</subject><subject>MAP Kinase Kinase Kinase 1</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Mitogen-Activated Protein Kinases - physiology</subject><subject>Molecular and cellular biology</subject><subject>Molecular biology</subject><subject>oncogenomics</subject><subject>Oncology</subject><subject>Phosphatase</subject><subject>Prostate cancer</subject><subject>Prostate-Specific Antigen - metabolism</subject><subject>Prostate-Specific Antigen - secretion</subject><subject>Prostatic Neoplasms</subject><subject>Protein Tyrosine Phosphatases - physiology</subject><subject>Protein-Serine-Threonine Kinases - antagonists & inhibitors</subject><subject>Proteins</subject><subject>Receptor, ErbB-2 - antagonists & inhibitors</subject><subject>Receptor, ErbB-2 - physiology</subject><subject>Signal transduction</subject><subject>Signal Transduction - physiology</subject><subject>Tumor Cells, Cultured</subject><subject>Up-Regulation - physiology</subject><issn>0950-9232</issn><issn>1476-5594</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqFkt-L1DAQx4so3t7pq48SFH3r3iRt8-Nxb7lTYdED9Tmk6bRm6aZr0p7435uyhQU5kUAyZD4zmZl8s-wVhTWFQl7H_Xrwdk0ZcOD8SbaipeB5VanyabYCVUGuWMEusssY9wAgFLDn2QVlFVeFYKvs122ob3JGouu86Z3viIvE-Yehf8AmGSRgN_VmnD33Xzckog04usHPPuObMHToc-cbPGLa_Eh-TAfjyTEMcTQjEmu8xUB2n7fmnmxzSYnFvo8vsmet6SO-XM6r7Pvd7bftx3z35cOn7WaX21LyMa8KVldILTNNWaKFRlHBpagKiaIGWXNOeY1oRGllQQUti4YZydBWbYOtFMVV9v6UNxX0c8I46oOLcwXG4zBFLQoASQv1X5BKrpQASOCbv8D9MIU0vKgZA8oBSpqgtyeoMz1q59thDMbOGfWGSkW5kJInav0IlVaDB2cHj61L948F2DTeGLDVx-AOJvzWFPSsBx33OulBL3pIAa-XYqf6gM0ZXwSQgHcLYKI1fRvSd7l45kougbO56-sTF5PLdxjOXf_j6T_4GMuX</recordid><startdate>20030206</startdate><enddate>20030206</enddate><creator>Lee, Ming-Shyue</creator><creator>Igawa, Tsukasa</creator><creator>Yuan, Ta-Chun</creator><creator>Zhang, Xiu-Qing</creator><creator>Lin, Fen-Fen</creator><creator>Lin, Ming-Fong</creator><general>Nature Publishing Group UK</general><general>Nature Publishing</general><general>Nature Publishing Group</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>7TM</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>M7P</scope><scope>MBDVC</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>20030206</creationdate><title>ErbB-2 signaling is involved in regulating PSA secretion in androgen-independent human prostate cancer LNCaP C-81 cells</title><author>Lee, Ming-Shyue ; Igawa, Tsukasa ; Yuan, Ta-Chun ; Zhang, Xiu-Qing ; Lin, Fen-Fen ; Lin, Ming-Fong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c486t-532b5e1c2ad44ec0d917687538e7b08b6616beea74c8317143d2a82ec5fdef873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Ablation</topic><topic>Acid Phosphatase</topic><topic>Androgens</topic><topic>Androgens - physiology</topic><topic>Antigens</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biological and medical sciences</topic><topic>Cell Biology</topic><topic>Cell Division - physiology</topic><topic>Cell physiology</topic><topic>Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes</topic><topic>Classical genetics, quantitative genetics, hybrids</topic><topic>Culture Media, Conditioned - metabolism</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Genetics of eukaryotes. Biological and molecular evolution</topic><topic>Genotype & phenotype</topic><topic>Human</topic><topic>Human Genetics</topic><topic>Humans</topic><topic>Internal Medicine</topic><topic>Kinases</topic><topic>Male</topic><topic>MAP Kinase Kinase Kinase 1</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Mitogen-Activated Protein Kinases - physiology</topic><topic>Molecular and cellular biology</topic><topic>Molecular biology</topic><topic>oncogenomics</topic><topic>Oncology</topic><topic>Phosphatase</topic><topic>Prostate cancer</topic><topic>Prostate-Specific Antigen - metabolism</topic><topic>Prostate-Specific Antigen - secretion</topic><topic>Prostatic Neoplasms</topic><topic>Protein Tyrosine Phosphatases - physiology</topic><topic>Protein-Serine-Threonine Kinases - antagonists & inhibitors</topic><topic>Proteins</topic><topic>Receptor, ErbB-2 - antagonists & inhibitors</topic><topic>Receptor, ErbB-2 - physiology</topic><topic>Signal transduction</topic><topic>Signal Transduction - physiology</topic><topic>Tumor Cells, Cultured</topic><topic>Up-Regulation - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lee, Ming-Shyue</creatorcontrib><creatorcontrib>Igawa, Tsukasa</creatorcontrib><creatorcontrib>Yuan, Ta-Chun</creatorcontrib><creatorcontrib>Zhang, Xiu-Qing</creatorcontrib><creatorcontrib>Lin, Fen-Fen</creatorcontrib><creatorcontrib>Lin, Ming-Fong</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Nucleic Acids Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Biological Science Database</collection><collection>Research Library (Corporate)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Oncogene</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lee, Ming-Shyue</au><au>Igawa, Tsukasa</au><au>Yuan, Ta-Chun</au><au>Zhang, Xiu-Qing</au><au>Lin, Fen-Fen</au><au>Lin, Ming-Fong</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>ErbB-2 signaling is involved in regulating PSA secretion in androgen-independent human prostate cancer LNCaP C-81 cells</atitle><jtitle>Oncogene</jtitle><stitle>Oncogene</stitle><addtitle>Oncogene</addtitle><date>2003-02-06</date><risdate>2003</risdate><volume>22</volume><issue>5</issue><spage>781</spage><epage>796</epage><pages>781-796</pages><issn>0950-9232</issn><eissn>1476-5594</eissn><coden>ONCNES</coden><abstract>The expression and secretion of prostate-specific antigen (PSA) are regulated by androgens in normal prostate secretory epithelial cells. In prostate cancer patients, the serum PSA level is usually elevated and cancer cells are initially responsive to androgens. However, those cancer cells become androgen-independent after androgen ablation therapy. In hormone-refractory cancer patients, even in an androgen-deprived environment, the circulation level of PSA rebounds and is constitutively elevated through a yet unknown mechanism. Tyrosine phosphorylation of ErbB-2 is involved in regulating the androgen-responsive phenotype of prostate cancer cells, and it is at least partly regulated by the cellular form of prostatic acid phosphatase (PAcP), a prostate-unique protein tyrosine phosphatase. We investigated the ErbB-2 signal pathway in androgen-independent PSA secretion. LNCaP C-81 cells, which are androgen-independent LNCaP cells lacking endogenous PAcP expression with a hypertyrosine phosphorylated ErbB-2, secreted a higher level of PSA in conditioned media than did androgen-sensitive LNCaP C-33 parental cells. A restored expression of cellular PAcP in C-81 cells was concurrent with a decrease in tyrophosphorylation of ErbB-2 and reduction of PSA secretion. Moreover, transient transfection of C-33 cells with the wild-type ErbB-2 or a constitutively active mutant of MEK1 cDNA resulted in an increased level of secreted PSA. The elevation of secreted PSA level by the forced expression of ErbB-2 was inhibited by an MEK inhibitor, PD98059. In C-81 cells, the expression of a dominant negative mutant of ErbB-2 reduced the secreted level of PSA. The inhibition of ErbB-2 or mitogen-activated protein (MAP) kinases by specific inhibitors AG879, AG825, or PD98059 led to a decrease in PSA secretion. Taken together, our data clearly indicate that the ErbB-2 signal pathway via MAP kinases (ERK1/2) is involved in regulating the secretion of PSA by androgen-independent human prostate cancer LNCaP C-81 cells in an androgen-depleted environment.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>12569372</pmid><doi>10.1038/sj.onc.1206066</doi><tpages>16</tpages></addata></record> |
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| subjects | Ablation Acid Phosphatase Androgens Androgens - physiology Antigens Apoptosis Biochemistry Biological and medical sciences Cell Biology Cell Division - physiology Cell physiology Cell transformation and carcinogenesis. Action of oncogenes and antioncogenes Classical genetics, quantitative genetics, hybrids Culture Media, Conditioned - metabolism Fundamental and applied biological sciences. Psychology Genetics of eukaryotes. Biological and molecular evolution Genotype & phenotype Human Human Genetics Humans Internal Medicine Kinases Male MAP Kinase Kinase Kinase 1 Medicine Medicine & Public Health Mitogen-Activated Protein Kinases - physiology Molecular and cellular biology Molecular biology oncogenomics Oncology Phosphatase Prostate cancer Prostate-Specific Antigen - metabolism Prostate-Specific Antigen - secretion Prostatic Neoplasms Protein Tyrosine Phosphatases - physiology Protein-Serine-Threonine Kinases - antagonists & inhibitors Proteins Receptor, ErbB-2 - antagonists & inhibitors Receptor, ErbB-2 - physiology Signal transduction Signal Transduction - physiology Tumor Cells, Cultured Up-Regulation - physiology |
| title | ErbB-2 signaling is involved in regulating PSA secretion in androgen-independent human prostate cancer LNCaP C-81 cells |
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