Silibinin inhibits prostate cancer invasion, motility and migration by suppressing vimentin and MMP-2 expression
Aim： Silibinin is known to exert growth inhibition and cell death together with cell cycle arrest and apoptosis in human prostate cancer cells. Whether silibinin could inhibit the invasion, motility and migration of prostate cancer cells remains largely unknown. This study was designed to evaluate t...
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| Veröffentlicht in: | Acta pharmacologica Sinica 2009-08, Vol.30 (8), p.1162-1168 |
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| creator | Wu, Kai-jie Zeng, Jin Zhu, Guo-dong Zhang, Lin-lin Zhang, Dong Li, Lei Fan, Jin-hai Wang, Xin-yang He, Da-lin |
| description | Aim： Silibinin is known to exert growth inhibition and cell death together with cell cycle arrest and apoptosis in human prostate cancer cells. Whether silibinin could inhibit the invasion, motility and migration of prostate cancer cells remains largely unknown. This study was designed to evaluate this efficacy and possible mechanisms using a novel highly bone metastatic ARCaPM cell model. Methods： Four prostate cancer cell lines, LNCaP, PC-3, DU145, and ARCaPM, were used in this study. These cells were treated with increasing concentrations of silibinin （50, 100, and 200 pmol/L） for different periods of time. After treatment, cell viabilities of four prostate cancer cells were compared by MTT assay. Alterations of ARCaPM cell invasion, motility and migration were assessed by cell invasion, motility and wound healing assays. The changes of vimentin expression were observed by Western blotting and immunofluorescence staining, and the expression of MMP-2, MMP-9, and uPA was analyzed by reverse transcription-polymerase chain reaction （RT-PCR）. Results： ARCaPM cells showed less sensitivity to the growth inhibition of pharmacological doses of silibinin than LNCaP, PC-3, and DU145 cells. However, silibinin exerted significant dose- and time-dependent inhibitory effects on the invasion, motility and migration of ARCaPM cells. Furthermore, the expression of vimentin and MMP-2, but not MMP-9 or uPA, was down-regulated in a dose-and timedependent manner after treatment of silibinin. Conclusion： This study shows that silibinin could inhibit the invasion, motility and migration of ARCaPM cells via down-regulation of vimentin and MMP-2 and therefore may be a promising agent against prostate cancer bone metastasis. |
| doi_str_mv | 10.1038/aps.2009.94 |
| format | Article |
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Whether silibinin could inhibit the invasion, motility and migration of prostate cancer cells remains largely unknown. This study was designed to evaluate this efficacy and possible mechanisms using a novel highly bone metastatic ARCaPM cell model. Methods： Four prostate cancer cell lines, LNCaP, PC-3, DU145, and ARCaPM, were used in this study. These cells were treated with increasing concentrations of silibinin （50, 100, and 200 pmol/L） for different periods of time. After treatment, cell viabilities of four prostate cancer cells were compared by MTT assay. Alterations of ARCaPM cell invasion, motility and migration were assessed by cell invasion, motility and wound healing assays. The changes of vimentin expression were observed by Western blotting and immunofluorescence staining, and the expression of MMP-2, MMP-9, and uPA was analyzed by reverse transcription-polymerase chain reaction （RT-PCR）. Results： ARCaPM cells showed less sensitivity to the growth inhibition of pharmacological doses of silibinin than LNCaP, PC-3, and DU145 cells. However, silibinin exerted significant dose- and time-dependent inhibitory effects on the invasion, motility and migration of ARCaPM cells. Furthermore, the expression of vimentin and MMP-2, but not MMP-9 or uPA, was down-regulated in a dose-and timedependent manner after treatment of silibinin. Conclusion： This study shows that silibinin could inhibit the invasion, motility and migration of ARCaPM cells via down-regulation of vimentin and MMP-2 and therefore may be a promising agent against prostate cancer bone metastasis.</description><identifier>ISSN: 1671-4083</identifier><identifier>EISSN: 1745-7254</identifier><identifier>DOI: 10.1038/aps.2009.94</identifier><identifier>PMID: 19578386</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>Antioxidants - therapeutic use ; Biomedical and Life Sciences ; Biomedicine ; Cell Line, Tumor ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Gene Expression Regulation, Neoplastic ; Humans ; Immunology ; Internal Medicine ; Male ; Matrix Metalloproteinase 2 - genetics ; Matrix Metalloproteinase 2 - metabolism ; Medical Microbiology ; MMP ; Neoplasm Invasiveness - prevention & control ; Original ; original-article ; Pharmacology/Toxicology ; Prostatic Neoplasms - pathology ; Silymarin - therapeutic use ; Vaccine ; Vimentin - genetics ; Vimentin - metabolism ; 前列腺 ; 水飞蓟 ; 波形蛋白 ; 癌细胞</subject><ispartof>Acta pharmacologica Sinica, 2009-08, Vol.30 (8), p.1162-1168</ispartof><rights>CPS and SIMM 2009</rights><rights>Copyright Nature Publishing Group Aug 2009</rights><rights>Copyright © 2009 CPS and SIMM 2009 CPS and SIMM</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c470t-e150c18449588d6b8869e6f51cb363fbee3732224816d9fa651b6ae98b6061713</citedby><cites>FETCH-LOGICAL-c470t-e150c18449588d6b8869e6f51cb363fbee3732224816d9fa651b6ae98b6061713</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://image.cqvip.com/vip1000/qk/95561A/95561A.jpg</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4006687/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4006687/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19578386$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Kai-jie</creatorcontrib><creatorcontrib>Zeng, Jin</creatorcontrib><creatorcontrib>Zhu, Guo-dong</creatorcontrib><creatorcontrib>Zhang, Lin-lin</creatorcontrib><creatorcontrib>Zhang, Dong</creatorcontrib><creatorcontrib>Li, Lei</creatorcontrib><creatorcontrib>Fan, Jin-hai</creatorcontrib><creatorcontrib>Wang, Xin-yang</creatorcontrib><creatorcontrib>He, Da-lin</creatorcontrib><title>Silibinin inhibits prostate cancer invasion, motility and migration by suppressing vimentin and MMP-2 expression</title><title>Acta pharmacologica Sinica</title><addtitle>Acta Pharmacol Sin</addtitle><addtitle>Acta Pharmacologica Sinica</addtitle><description>Aim： Silibinin is known to exert growth inhibition and cell death together with cell cycle arrest and apoptosis in human prostate cancer cells. Whether silibinin could inhibit the invasion, motility and migration of prostate cancer cells remains largely unknown. This study was designed to evaluate this efficacy and possible mechanisms using a novel highly bone metastatic ARCaPM cell model. Methods： Four prostate cancer cell lines, LNCaP, PC-3, DU145, and ARCaPM, were used in this study. These cells were treated with increasing concentrations of silibinin （50, 100, and 200 pmol/L） for different periods of time. After treatment, cell viabilities of four prostate cancer cells were compared by MTT assay. Alterations of ARCaPM cell invasion, motility and migration were assessed by cell invasion, motility and wound healing assays. The changes of vimentin expression were observed by Western blotting and immunofluorescence staining, and the expression of MMP-2, MMP-9, and uPA was analyzed by reverse transcription-polymerase chain reaction （RT-PCR）. Results： ARCaPM cells showed less sensitivity to the growth inhibition of pharmacological doses of silibinin than LNCaP, PC-3, and DU145 cells. However, silibinin exerted significant dose- and time-dependent inhibitory effects on the invasion, motility and migration of ARCaPM cells. Furthermore, the expression of vimentin and MMP-2, but not MMP-9 or uPA, was down-regulated in a dose-and timedependent manner after treatment of silibinin. Conclusion： This study shows that silibinin could inhibit the invasion, motility and migration of ARCaPM cells via down-regulation of vimentin and MMP-2 and therefore may be a promising agent against prostate cancer bone metastasis.</description><subject>Antioxidants - therapeutic use</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell Line, Tumor</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Gene Expression Regulation, Neoplastic</subject><subject>Humans</subject><subject>Immunology</subject><subject>Internal Medicine</subject><subject>Male</subject><subject>Matrix Metalloproteinase 2 - genetics</subject><subject>Matrix Metalloproteinase 2 - metabolism</subject><subject>Medical Microbiology</subject><subject>MMP</subject><subject>Neoplasm Invasiveness - prevention & control</subject><subject>Original</subject><subject>original-article</subject><subject>Pharmacology/Toxicology</subject><subject>Prostatic Neoplasms - pathology</subject><subject>Silymarin - therapeutic use</subject><subject>Vaccine</subject><subject>Vimentin - genetics</subject><subject>Vimentin - metabolism</subject><subject>前列腺</subject><subject>水飞蓟</subject><subject>波形蛋白</subject><subject>癌细胞</subject><issn>1671-4083</issn><issn>1745-7254</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptks-P1CAcxRujcX_oybshHrzsdoTy-7KJ2fgr2Y0m6plQhnZYW-hCO3H-e7-TmbhqPEF4Hx4PHlX1guAVwVS9sVNZNRjrlWaPqlMiGa9lw9ljmAtJaoYVPanOSrnDmDaU6KfVCdFcKqrEaTV9DUNoQwwRhbiB2VzQlFOZ7eyRs9H5DMLWlpDiJRrTDPi8Qzau0Rj6bGdYR-0OlWWasi8lxB5tw-jjDI576vb2S90g__OgpvisetLZofjnx_G8-v7-3bfrj_XN5w-frt_e1I5JPNeecOyIYkxzpdaiVUpoLzpOXEsF7VrvqaRN0zBFxFp3VnDSCuu1agUWRBJ6Xl0dfKelHf3aQaJsBzPlMNq8M8kG87cSw8b0aWsYxkIoCQavjwY53S--zGYMxflhsNGnpRghOVdMawBf_QPepSVHuJxpCMUNxKEAXRwgB49bsu9-JyHY7Gs0UKPZ12g0A_rln-Ef2GNvAFwegAJS7H1-OPP_fseIbpNifw87TGvdjy4M3lBCJNfwSX4BQrS0qQ</recordid><startdate>20090801</startdate><enddate>20090801</enddate><creator>Wu, Kai-jie</creator><creator>Zeng, Jin</creator><creator>Zhu, Guo-dong</creator><creator>Zhang, Lin-lin</creator><creator>Zhang, Dong</creator><creator>Li, Lei</creator><creator>Fan, Jin-hai</creator><creator>Wang, Xin-yang</creator><creator>He, Da-lin</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>2RA</scope><scope>92L</scope><scope>CQIGP</scope><scope>W94</scope><scope>WU4</scope><scope>~WA</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>7QP</scope><scope>7QR</scope><scope>7T5</scope><scope>7TK</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</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>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20090801</creationdate><title>Silibinin inhibits prostate cancer invasion, motility and migration by suppressing vimentin and MMP-2 expression</title><author>Wu, Kai-jie ; Zeng, Jin ; Zhu, Guo-dong ; Zhang, Lin-lin ; Zhang, Dong ; Li, Lei ; Fan, Jin-hai ; Wang, Xin-yang ; He, Da-lin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c470t-e150c18449588d6b8869e6f51cb363fbee3732224816d9fa651b6ae98b6061713</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Antioxidants - therapeutic use</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell Line, Tumor</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Gene Expression Regulation, Neoplastic</topic><topic>Humans</topic><topic>Immunology</topic><topic>Internal Medicine</topic><topic>Male</topic><topic>Matrix Metalloproteinase 2 - genetics</topic><topic>Matrix Metalloproteinase 2 - metabolism</topic><topic>Medical Microbiology</topic><topic>MMP</topic><topic>Neoplasm Invasiveness - prevention & control</topic><topic>Original</topic><topic>original-article</topic><topic>Pharmacology/Toxicology</topic><topic>Prostatic Neoplasms - pathology</topic><topic>Silymarin - therapeutic use</topic><topic>Vaccine</topic><topic>Vimentin - genetics</topic><topic>Vimentin - metabolism</topic><topic>前列腺</topic><topic>水飞蓟</topic><topic>波形蛋白</topic><topic>癌细胞</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wu, Kai-jie</creatorcontrib><creatorcontrib>Zeng, Jin</creatorcontrib><creatorcontrib>Zhu, Guo-dong</creatorcontrib><creatorcontrib>Zhang, Lin-lin</creatorcontrib><creatorcontrib>Zhang, Dong</creatorcontrib><creatorcontrib>Li, Lei</creatorcontrib><creatorcontrib>Fan, Jin-hai</creatorcontrib><creatorcontrib>Wang, Xin-yang</creatorcontrib><creatorcontrib>He, Da-lin</creatorcontrib><collection>中文科技期刊数据库</collection><collection>中文科技期刊数据库-CALIS站点</collection><collection>中文科技期刊数据库-7.0平台</collection><collection>中文科技期刊数据库-自然科学</collection><collection>中文科技期刊数据库-自然科学-生物科学</collection><collection>中文科技期刊数据库- 镜像站点</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>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Neurosciences 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>Medical Database (Alumni Edition)</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>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>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>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</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>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Acta pharmacologica Sinica</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Kai-jie</au><au>Zeng, Jin</au><au>Zhu, Guo-dong</au><au>Zhang, Lin-lin</au><au>Zhang, Dong</au><au>Li, Lei</au><au>Fan, Jin-hai</au><au>Wang, Xin-yang</au><au>He, Da-lin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Silibinin inhibits prostate cancer invasion, motility and migration by suppressing vimentin and MMP-2 expression</atitle><jtitle>Acta pharmacologica Sinica</jtitle><stitle>Acta Pharmacol Sin</stitle><addtitle>Acta Pharmacologica Sinica</addtitle><date>2009-08-01</date><risdate>2009</risdate><volume>30</volume><issue>8</issue><spage>1162</spage><epage>1168</epage><pages>1162-1168</pages><issn>1671-4083</issn><eissn>1745-7254</eissn><abstract>Aim： Silibinin is known to exert growth inhibition and cell death together with cell cycle arrest and apoptosis in human prostate cancer cells. Whether silibinin could inhibit the invasion, motility and migration of prostate cancer cells remains largely unknown. This study was designed to evaluate this efficacy and possible mechanisms using a novel highly bone metastatic ARCaPM cell model. Methods： Four prostate cancer cell lines, LNCaP, PC-3, DU145, and ARCaPM, were used in this study. These cells were treated with increasing concentrations of silibinin （50, 100, and 200 pmol/L） for different periods of time. After treatment, cell viabilities of four prostate cancer cells were compared by MTT assay. Alterations of ARCaPM cell invasion, motility and migration were assessed by cell invasion, motility and wound healing assays. The changes of vimentin expression were observed by Western blotting and immunofluorescence staining, and the expression of MMP-2, MMP-9, and uPA was analyzed by reverse transcription-polymerase chain reaction （RT-PCR）. Results： ARCaPM cells showed less sensitivity to the growth inhibition of pharmacological doses of silibinin than LNCaP, PC-3, and DU145 cells. However, silibinin exerted significant dose- and time-dependent inhibitory effects on the invasion, motility and migration of ARCaPM cells. Furthermore, the expression of vimentin and MMP-2, but not MMP-9 or uPA, was down-regulated in a dose-and timedependent manner after treatment of silibinin. Conclusion： This study shows that silibinin could inhibit the invasion, motility and migration of ARCaPM cells via down-regulation of vimentin and MMP-2 and therefore may be a promising agent against prostate cancer bone metastasis.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>19578386</pmid><doi>10.1038/aps.2009.94</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antioxidants - therapeutic use Biomedical and Life Sciences Biomedicine Cell Line, Tumor Cell Movement - drug effects Cell Proliferation - drug effects Gene Expression Regulation, Neoplastic Humans Immunology Internal Medicine Male Matrix Metalloproteinase 2 - genetics Matrix Metalloproteinase 2 - metabolism Medical Microbiology MMP Neoplasm Invasiveness - prevention & control Original original-article Pharmacology/Toxicology Prostatic Neoplasms - pathology Silymarin - therapeutic use Vaccine Vimentin - genetics Vimentin - metabolism 前列腺 水飞蓟 波形蛋白 癌细胞 |
| title | Silibinin inhibits prostate cancer invasion, motility and migration by suppressing vimentin and MMP-2 expression |
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