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10.1002/mc.22135 http://scihub22266oqcxt.onion/10.1002/mc.22135 C4208986!4208986 !24615813     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24615813 &cmd=llinks): Failed to open stream: HTTP request failed! 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Silibinin prevents prostate cancer cell-mediated differentiation of naïve fibroblasts into cancer-associated fibroblast phenotype by targeting TGF ?2 |pdf=|usr=}}{{24615813 }} gab.com Text Silibinin prevents prostate cancer cell-mediated differentiation of naïve fibroblasts into cancer-associated fibroblast phenotype by targeting TGF 2 JO: Mol Carcinog http://www.kidney.de/pget.php?&tw=1&pmid=24615813 #FOAvip Tumor microenvironment (TM) is an essential element in prostate cancer (PCA), offering unique opportunities for its prevention. TM includes naïve fibroblasts that are recruited by nascent neoplastic lesion and altered into 'cancer-associated fibroblasts' (CAFs) that promote PCA. A better understanding and targeting of interaction between PCA cells and fibroblasts and inhibiting CAF phenotype through non-toxic agents are novel approaches to prevent PCA progression. One well-studied cancer chemopreventive agent is silibinin, and thus, we examined its efficacy against PCA cells-mediated differentiation of naïve fibroblasts into a myofibroblastic-phenotype similar to that found in CAFs. Silibinin's direct inhibitory effect on the phenotype of CAFs derived directly from PCA patients was also assessed. Human prostate stromal cells (PrSCs) exposed to control conditioned media (CCM) from human PCA PC3 cells showed more invasiveness, with increased alpha-smooth muscle actin (?-SMA) and vimentin expression, and differentiation into a phenotype we identified in CAFs. Importantly, silibinin (at physiologically achievable concentrations) inhibited ?-SMA expression and invasiveness in differentiated fibroblasts and prostate CAFs directly, as well as indirectly by targeting PCA cells. The observed increase in ?-SMA and CAF-like phenotype was transforming growth factor (TGF) ?2 dependent, which was strongly inhibited by silibinin. Furthermore, induction of ?-SMA and CAF phenotype by CCM were also strongly inhibited by a TGF?2-neutralizing antibody. The inhibitory effect of silibinin on TGF?2 expression and CAF-like biomarkers was also observed in PC3 tumors. Together, these findings highlight the potential usefulness of silibinin in PCA prevention through targeting the CAF phenotype in the prostate TM. Twit Text FOAVip Silibinin prevents prostate cancer cell-mediated differentiation of naïve fibroblasts into cancer-associated fibroblast phenotype by targeting TGF 2 ????Mol Carcinog http://www.kidney.de/pget.php?&tw=1&pmid=24615813 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24615813 #FOAvip English Wikipedia <ref>{{Cite pmid|24615813 }}</ref> Silibinin prevents prostate cancer cell-mediated differentiation of naïve fibroblasts into cancer-associated fibroblast phenotype by targeting TGF ?2 #MMPMID24615813 Ting HJ ; Deep G ; Jain AK ; Cimic A ; Sirintrapun J ; Romero LM ; Cramer SD ; Agarwal C ; Agarwal R Mol Carcinog 2015[Sep]; 54 (9 ): 730-41 PMID24615813 show ga Tumor microenvironment (TM) is an essential element in prostate cancer (PCA), offering unique opportunities for its prevention. TM includes naïve fibroblasts that are recruited by nascent neoplastic lesion and altered into 'cancer-associated fibroblasts' (CAFs) that promote PCA. A better understanding and targeting of interaction between PCA cells and fibroblasts and inhibiting CAF phenotype through non-toxic agents are novel approaches to prevent PCA progression. One well-studied cancer chemopreventive agent is silibinin, and thus, we examined its efficacy against PCA cells-mediated differentiation of naïve fibroblasts into a myofibroblastic-phenotype similar to that found in CAFs. Silibinin's direct inhibitory effect on the phenotype of CAFs derived directly from PCA patients was also assessed. Human prostate stromal cells (PrSCs) exposed to control conditioned media (CCM) from human PCA PC3 cells showed more invasiveness, with increased alpha-smooth muscle actin (?-SMA) and vimentin expression, and differentiation into a phenotype we identified in CAFs. Importantly, silibinin (at physiologically achievable concentrations) inhibited ?-SMA expression and invasiveness in differentiated fibroblasts and prostate CAFs directly, as well as indirectly by targeting PCA cells. The observed increase in ?-SMA and CAF-like phenotype was transforming growth factor (TGF) ?2 dependent, which was strongly inhibited by silibinin. Furthermore, induction of ?-SMA and CAF phenotype by CCM were also strongly inhibited by a TGF?2-neutralizing antibody. The inhibitory effect of silibinin on TGF?2 expression and CAF-like biomarkers was also observed in PC3 tumors. Together, these findings highlight the potential usefulness of silibinin in PCA prevention through targeting the CAF phenotype in the prostate TM. |Anticarcinogenic Agents/chemistry/*pharmacology [MESH] |Antioxidants/chemistry/pharmacology [MESH] |Cell Differentiation/drug effects [MESH] |Cell Line, Tumor [MESH] |Fibroblasts/*drug effects/metabolism/pathology [MESH] |Humans [MESH] |Male [MESH] |Prostate/cytology/*drug effects/metabolism/pathology [MESH] |Prostatic Neoplasms/*metabolism/pathology/*prevention & control [MESH] |Silybin [MESH] |Silybum marianum/chemistry [MESH] |Silymarin/chemistry/*pharmacology [MESH]Silibinin prevents prostate cancer cell-mediated differentiation of na(epmc).pdf DeepDyve Pubget Overpricing