Finasteride induces apoptosis via Bcl-2, Bcl-xL, Bax and caspase-3 proteins in LNCaP human prostate cancer cell line
We investigated the effects of finasteride, a 5alpha-reductase inhibitor, on cell death machinery through the induction of apoptosis in an in vitro model for prostate cancer. Finasteride treatment of the LNCaP hormone-dependent human prostate cancer cell line caused the loss of cell viability and ac...
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| Veröffentlicht in: | International journal of oncology 2008-04, Vol.32 (4), p.919-924 |
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| container_title | International journal of oncology |
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| creator | GOLBANO, Jesus M LOPEZ-APARICIO, Pilar RECIO, Maria N PEREZ-ALBARSANZ, Miguel A |
| description | We investigated the effects of finasteride, a 5alpha-reductase inhibitor, on cell death machinery through the induction of apoptosis in an in vitro model for prostate cancer. Finasteride treatment of the LNCaP hormone-dependent human prostate cancer cell line caused the loss of cell viability and accelerated apoptosis in a concentration-dependent manner. The contents of immunoreactive procaspase-3 were examined by immunoblot analysis and the results suggest that the apoptosis induced by finasteride involves the increase of caspase-3 activity. Early cell changes that occur during apoptosis are associated with mitochondrial changes mediated by members of the Bcl-2 family of proteins. Therefore, Bcl-2, Bcl-xL and Bax were evaluated by the Western blot analysis. The immunoreactivity for pro-apoptotic Bax was markedly increased whereas antiapoptotic Bcl-2 and Bcl-xL expression was significantly reduced after incubation of cells with finasteride. These findings suggest that finasteride induces apoptosis in LNCaP cells via proteins of the Bcl-2 and caspase family. |
| doi_str_mv | 10.3892/ijo.32.4.919 |
| format | Article |
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Finasteride treatment of the LNCaP hormone-dependent human prostate cancer cell line caused the loss of cell viability and accelerated apoptosis in a concentration-dependent manner. The contents of immunoreactive procaspase-3 were examined by immunoblot analysis and the results suggest that the apoptosis induced by finasteride involves the increase of caspase-3 activity. Early cell changes that occur during apoptosis are associated with mitochondrial changes mediated by members of the Bcl-2 family of proteins. Therefore, Bcl-2, Bcl-xL and Bax were evaluated by the Western blot analysis. The immunoreactivity for pro-apoptotic Bax was markedly increased whereas antiapoptotic Bcl-2 and Bcl-xL expression was significantly reduced after incubation of cells with finasteride. These findings suggest that finasteride induces apoptosis in LNCaP cells via proteins of the Bcl-2 and caspase family.</description><identifier>ISSN: 1019-6439</identifier><identifier>EISSN: 1791-2423</identifier><identifier>DOI: 10.3892/ijo.32.4.919</identifier><identifier>PMID: 18360719</identifier><language>eng</language><publisher>Athens: Editorial Academy of the International Journal of Oncology</publisher><subject>Apoptosis - drug effects ; bcl-2-Associated X Protein - physiology ; bcl-X Protein - physiology ; Biological and medical sciences ; Caspase 3 - physiology ; Cell Line, Tumor ; Cholestenone 5 alpha-Reductase - antagonists & inhibitors ; Enzyme Inhibitors - pharmacology ; Finasteride - pharmacology ; Humans ; Male ; Medical sciences ; Nephrology. Urinary tract diseases ; Prostatic Neoplasms - drug therapy ; Prostatic Neoplasms - pathology ; Proto-Oncogene Proteins c-bcl-2 - physiology ; Tumors ; Tumors of the urinary system ; Urinary tract. 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Finasteride treatment of the LNCaP hormone-dependent human prostate cancer cell line caused the loss of cell viability and accelerated apoptosis in a concentration-dependent manner. The contents of immunoreactive procaspase-3 were examined by immunoblot analysis and the results suggest that the apoptosis induced by finasteride involves the increase of caspase-3 activity. Early cell changes that occur during apoptosis are associated with mitochondrial changes mediated by members of the Bcl-2 family of proteins. Therefore, Bcl-2, Bcl-xL and Bax were evaluated by the Western blot analysis. The immunoreactivity for pro-apoptotic Bax was markedly increased whereas antiapoptotic Bcl-2 and Bcl-xL expression was significantly reduced after incubation of cells with finasteride. These findings suggest that finasteride induces apoptosis in LNCaP cells via proteins of the Bcl-2 and caspase family.</description><subject>Apoptosis - drug effects</subject><subject>bcl-2-Associated X Protein - physiology</subject><subject>bcl-X Protein - physiology</subject><subject>Biological and medical sciences</subject><subject>Caspase 3 - physiology</subject><subject>Cell Line, Tumor</subject><subject>Cholestenone 5 alpha-Reductase - antagonists & inhibitors</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Finasteride - pharmacology</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Prostatic Neoplasms - drug therapy</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Proto-Oncogene Proteins c-bcl-2 - physiology</subject><subject>Tumors</subject><subject>Tumors of the urinary system</subject><subject>Urinary tract. 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Urinary tract diseases</topic><topic>Prostatic Neoplasms - drug therapy</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Proto-Oncogene Proteins c-bcl-2 - physiology</topic><topic>Tumors</topic><topic>Tumors of the urinary system</topic><topic>Urinary tract. Prostate gland</topic><toplevel>online_resources</toplevel><creatorcontrib>GOLBANO, Jesus M</creatorcontrib><creatorcontrib>LOPEZ-APARICIO, Pilar</creatorcontrib><creatorcontrib>RECIO, Maria N</creatorcontrib><creatorcontrib>PEREZ-ALBARSANZ, Miguel A</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>Oncogenes and Growth Factors Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>International journal of oncology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>GOLBANO, Jesus M</au><au>LOPEZ-APARICIO, Pilar</au><au>RECIO, Maria N</au><au>PEREZ-ALBARSANZ, Miguel A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Finasteride induces apoptosis via Bcl-2, Bcl-xL, Bax and caspase-3 proteins in LNCaP human prostate cancer cell line</atitle><jtitle>International journal of oncology</jtitle><addtitle>Int J Oncol</addtitle><date>2008-04</date><risdate>2008</risdate><volume>32</volume><issue>4</issue><spage>919</spage><epage>924</epage><pages>919-924</pages><issn>1019-6439</issn><eissn>1791-2423</eissn><abstract>We investigated the effects of finasteride, a 5alpha-reductase inhibitor, on cell death machinery through the induction of apoptosis in an in vitro model for prostate cancer. Finasteride treatment of the LNCaP hormone-dependent human prostate cancer cell line caused the loss of cell viability and accelerated apoptosis in a concentration-dependent manner. The contents of immunoreactive procaspase-3 were examined by immunoblot analysis and the results suggest that the apoptosis induced by finasteride involves the increase of caspase-3 activity. Early cell changes that occur during apoptosis are associated with mitochondrial changes mediated by members of the Bcl-2 family of proteins. Therefore, Bcl-2, Bcl-xL and Bax were evaluated by the Western blot analysis. The immunoreactivity for pro-apoptotic Bax was markedly increased whereas antiapoptotic Bcl-2 and Bcl-xL expression was significantly reduced after incubation of cells with finasteride. 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| source | Spandidos Publications Journals; MEDLINE; EZB-FREE-00999 freely available EZB journals |
| subjects | Apoptosis - drug effects bcl-2-Associated X Protein - physiology bcl-X Protein - physiology Biological and medical sciences Caspase 3 - physiology Cell Line, Tumor Cholestenone 5 alpha-Reductase - antagonists & inhibitors Enzyme Inhibitors - pharmacology Finasteride - pharmacology Humans Male Medical sciences Nephrology. Urinary tract diseases Prostatic Neoplasms - drug therapy Prostatic Neoplasms - pathology Proto-Oncogene Proteins c-bcl-2 - physiology Tumors Tumors of the urinary system Urinary tract. Prostate gland |
| title | Finasteride induces apoptosis via Bcl-2, Bcl-xL, Bax and caspase-3 proteins in LNCaP human prostate cancer cell line |
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