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10.18632/oncotarget.10483 http://scihub22266oqcxt.onion/10.18632/oncotarget.10483 C5342411!5342411!27409422     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 298.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27409422.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Oncotarget 2016 ; 7 (34): 55191-210 Nephropedia Template TP {{tp|p=27409422|t=2016. 14-3-3? and aPKC-? synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3?/snail signaling pathway |pdf=|usr=}}{{27409422}} gab.com Text 14-3-3 and aPKC- synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3 /snail signaling pathway JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27409422 #FOAvip Cholangiocarcinoma (CCA) invasion and metastasis are the primary causes of poor survival rates in patients. The epithelial-mesenchymal transition (EMT) is a crucial step in cancer invasion and metastasis. However, it is still unclear of the molecular mechanism. In this study, the expression of 14-3-3? and atypical protein kinase C-? (aPKC-?) was further detected in CCA tissues and cell lines. Meanwhile, we established the EMT model of CCA cells and investigated 14-3-3? and aPKC-? co-regulatory effect on the EMT in vitro and in vivo. Further, we identified the downstream molecular glycogen synthase kinase 3 beta (GSK-3?)/Snail signalling pathway that contribute to regulating the EMT. Our data showed that the expression of 14-3-3? and aPKC-? was synergistically increased in CCA tissues compared with adjacent noncancerous tissues and was intimately associated with differentiation and the tumour-node-metastasis (TNM) stage. Multivariate Cox regression analysis indicated that high 14-3-3? and aPKC-? expression separately predicted a poor prognosis and were independent prognostic indicators in patients with CCA. The CO-IP experiment confirmed that the mutual binding relationship between 14-3-3? and aPKC-?. Small interfering RNAs and siRNA rescue experiment demonstrated that 14-3-3? and aPKC-? regulated each other. In addition, 14-3-3? and aPKC-? pretreatment by si-RNA inhibit the phosphorylated GSK-3? and Snail expression during EMT. Meanwhile, silence of 14-3-3? or aPKC-? suppressed CCA cells migration, metastasis and proliferation in vitro and in vivo. Our study demonstrates that 14-3-3? and aPKC-? synergistically facilitate EMT of CCA via GSK-3?/Snail signalling pathway, and may be potential therapeutic target for CCA. Twit Text FOAVip 14-3-3 and aPKC- synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3 /snail signaling pathway ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27409422 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27409422 #FOAvip English Wikipedia <ref>{{Cite pmid|27409422}}</ref> 14-3-3? and aPKC-? synergistically facilitate epithelial-mesenchymal transition of cholangiocarcinoma via GSK-3?/snail signaling pathway #MMPMID27409422 Yang Y; Liu Y; He Jc; Wang Jm; Schemmer P; Ma Cq; Qian Yw; Yao W; Zhang J; Qi Wp; Fu Y; Feng W; Yang T Oncotarget 2016[Aug]; 7 (34): 55191-210 PMID27409422show ga Cholangiocarcinoma (CCA) invasion and metastasis are the primary causes of poor survival rates in patients. The epithelial-mesenchymal transition (EMT) is a crucial step in cancer invasion and metastasis. However, it is still unclear of the molecular mechanism. In this study, the expression of 14-3-3? and atypical protein kinase C-? (aPKC-?) was further detected in CCA tissues and cell lines. Meanwhile, we established the EMT model of CCA cells and investigated 14-3-3? and aPKC-? co-regulatory effect on the EMT in vitro and in vivo. Further, we identified the downstream molecular glycogen synthase kinase 3 beta (GSK-3?)/Snail signalling pathway that contribute to regulating the EMT. Our data showed that the expression of 14-3-3? and aPKC-? was synergistically increased in CCA tissues compared with adjacent noncancerous tissues and was intimately associated with differentiation and the tumour-node-metastasis (TNM) stage. Multivariate Cox regression analysis indicated that high 14-3-3? and aPKC-? expression separately predicted a poor prognosis and were independent prognostic indicators in patients with CCA. The CO-IP experiment confirmed that the mutual binding relationship between 14-3-3? and aPKC-?. Small interfering RNAs and siRNA rescue experiment demonstrated that 14-3-3? and aPKC-? regulated each other. In addition, 14-3-3? and aPKC-? pretreatment by si-RNA inhibit the phosphorylated GSK-3? and Snail expression during EMT. Meanwhile, silence of 14-3-3? or aPKC-? suppressed CCA cells migration, metastasis and proliferation in vitro and in vivo. Our study demonstrates that 14-3-3? and aPKC-? synergistically facilitate EMT of CCA via GSK-3?/Snail signalling pathway, and may be potential therapeutic target for CCA. ä14-3-3? and aPKC-? synergistically facilitate epithelial-mesenchymal t(epmc).pdf DeepDyve Pubget Overpricing