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10.1371/journal.pone.0121319 http://scihub22266oqcxt.onion/10.1371/journal.pone.0121319 C4370615!4370615 !25799022     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25799022 &cmd=llinks): Failed to open stream: HTTP request failed! 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S100 calcium-binding protein A6 promotes epithelial-mesenchymal transition through ?-catenin in pancreatic cancer cell line |pdf=|usr=}}{{25799022 }} gab.com Text S100 calcium-binding protein A6 promotes epithelial-mesenchymal transition through -catenin in pancreatic cancer cell line JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25799022 #FOAvip The pathogenesis of pancreatic ductal adenocarcinoma (PDAC) remains poorly understood. S100 calcium-binding protein A6 (S100A6) has been associated with PDAC; however, the effect of S100A6 on PDAC migration and invasion has not yet been explored. In this study, Panc-1 cells were transfected with a plasmid to induce overexpression of S100A6, and ?-catenin was knocked down using a specific short hairpin RNA (shRNA). The wound-healing and Transwell assays demonstrated that S100A6 promoted PDAC cell migration and invasion. Furthermore, ?-catenin shRNA inhibited the migration and invasion of PDAC cells. We confirmed that S100A6 induces PDAC cell migration and invasion via activation of ?-catenin in vitro. Assessment of mRNA and protein levels revealed that S100A6 induces increased expression of ?-catenin, N-cadherin and vimentin, and decreased expression of E-cadherin in PDAC cells. ?-catenin shRNA also altered the expression of epithelial-mesenchymal transition (EMT)-related markers in PDAC cells. Specifically, expression of E-cadherin was increased, whereas expression of N-cadherin and vimentin was decreased. Finally, we demonstrated that S100A6 alters the expression of EMT-related markers via ?-catenin activation. In conclusion, S100A6 induces EMT and promotes cell migration and invasion in a ?-catenin-dependent manner. S100A6 may therefore represent a novel potential therapeutic target for the treatment of pancreatic cancer. Twit Text FOAVip S100 calcium-binding protein A6 promotes epithelial-mesenchymal transition through -catenin in pancreatic cancer cell line ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25799022 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25799022 #FOAvip English Wikipedia <ref>{{Cite pmid|25799022 }}</ref> S100 calcium-binding protein A6 promotes epithelial-mesenchymal transition through ?-catenin in pancreatic cancer cell line #MMPMID25799022 Chen X ; Liu X ; Lang H ; Zhang S ; Luo Y ; Zhang J PLoS One 2015[]; 10 (3 ): e0121319 PMID25799022 show ga The pathogenesis of pancreatic ductal adenocarcinoma (PDAC) remains poorly understood. S100 calcium-binding protein A6 (S100A6) has been associated with PDAC; however, the effect of S100A6 on PDAC migration and invasion has not yet been explored. In this study, Panc-1 cells were transfected with a plasmid to induce overexpression of S100A6, and ?-catenin was knocked down using a specific short hairpin RNA (shRNA). The wound-healing and Transwell assays demonstrated that S100A6 promoted PDAC cell migration and invasion. Furthermore, ?-catenin shRNA inhibited the migration and invasion of PDAC cells. We confirmed that S100A6 induces PDAC cell migration and invasion via activation of ?-catenin in vitro. Assessment of mRNA and protein levels revealed that S100A6 induces increased expression of ?-catenin, N-cadherin and vimentin, and decreased expression of E-cadherin in PDAC cells. ?-catenin shRNA also altered the expression of epithelial-mesenchymal transition (EMT)-related markers in PDAC cells. Specifically, expression of E-cadherin was increased, whereas expression of N-cadherin and vimentin was decreased. Finally, we demonstrated that S100A6 alters the expression of EMT-related markers via ?-catenin activation. In conclusion, S100A6 induces EMT and promotes cell migration and invasion in a ?-catenin-dependent manner. S100A6 may therefore represent a novel potential therapeutic target for the treatment of pancreatic cancer. |*Epithelial-Mesenchymal Transition [MESH] |Adenocarcinoma/*metabolism [MESH] |Cell Cycle Proteins/genetics/*metabolism [MESH] |Cell Line, Tumor [MESH] |Cell Movement [MESH] |Humans [MESH] |Pancreatic Neoplasms/*metabolism [MESH] |S100 Calcium Binding Protein A6 [MESH] |S100 Proteins/genetics/*metabolism [MESH]S100 calcium-binding protein A6 promotes epithelial-mesenchymal transi(epmc).pdf DeepDyve Pubget Overpricing