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10.1158/0008-5472.CAN-16-0438 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-16-0438 C5315491!5315491 !27659045     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27659045 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215       Cancer+Res 2016 ; 76 (22 ): 6543-6554 Nephropedia Template TP {{tp|p=27659045 |t=2016. IGFBP2 Activates the NF-?B Pathway to Drive Epithelial-Mesenchymal Transition and Invasive Character in Pancreatic Ductal Adenocarcinoma |pdf=|usr=}}{{27659045 }} gab.com Text IGFBP2 Activates the NF- B Pathway to Drive Epithelial-Mesenchymal Transition and Invasive Character in Pancreatic Ductal Adenocarcinoma JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27659045 #FOAvip The molecular basis underlying the particularly aggressive nature of pancreatic ductal adenocarcinoma (PDAC) still remains unclear. Here we report evidence that the insulin-like growth factor-binding protein IGFBP2 acts as a potent oncogene to drive its extremely malignant character. We found that elevated IGFBP2 expression in primary tumors was associated with lymph node metastasis and shorter survival in patients with PDAC. Enforced expression of IGFBP2 promoted invasion and metastasis of PDAC cells in vitro and in vivo by inducing NF-?B-dependent epithelial-mesenchymal transition (EMT). Mechanistic investigations revealed that IGFBP2 induced the nuclear translocation and phosphorylation of the p65 NF-?B subunit through the PI3K/Akt/IKK? pathway. Conversely, enforced expression of PTEN blunted this signaling pathway and restored an epithelial phenotype to PDAC cells in the presence of overexpressed IGFBP2. Overall, our results identify IGFBP2 as a pivotal regulator of an EMT axis in PDAC, the activation of which is sufficient to confer the characteristically aggressive clinical features of this disease. Cancer Res; 76(22); 6543-54. ©2016 AACR. Twit Text FOAVip IGFBP2 Activates the NF- B Pathway to Drive Epithelial-Mesenchymal Transition and Invasive Character in Pancreatic Ductal Adenocarcinoma ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=27659045 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27659045 #FOAvip English Wikipedia <ref>{{Cite pmid|27659045 }}</ref> IGFBP2 Activates the NF-?B Pathway to Drive Epithelial-Mesenchymal Transition and Invasive Character in Pancreatic Ductal Adenocarcinoma #MMPMID27659045 Gao S ; Sun Y ; Zhang X ; Hu L ; Liu Y ; Chua CY ; Phillips LM ; Ren H ; Fleming JB ; Wang H ; Chiao PJ ; Hao J ; Zhang W Cancer Res 2016[Nov]; 76 (22 ): 6543-6554 PMID27659045 show ga The molecular basis underlying the particularly aggressive nature of pancreatic ductal adenocarcinoma (PDAC) still remains unclear. Here we report evidence that the insulin-like growth factor-binding protein IGFBP2 acts as a potent oncogene to drive its extremely malignant character. We found that elevated IGFBP2 expression in primary tumors was associated with lymph node metastasis and shorter survival in patients with PDAC. Enforced expression of IGFBP2 promoted invasion and metastasis of PDAC cells in vitro and in vivo by inducing NF-?B-dependent epithelial-mesenchymal transition (EMT). Mechanistic investigations revealed that IGFBP2 induced the nuclear translocation and phosphorylation of the p65 NF-?B subunit through the PI3K/Akt/IKK? pathway. Conversely, enforced expression of PTEN blunted this signaling pathway and restored an epithelial phenotype to PDAC cells in the presence of overexpressed IGFBP2. Overall, our results identify IGFBP2 as a pivotal regulator of an EMT axis in PDAC, the activation of which is sufficient to confer the characteristically aggressive clinical features of this disease. Cancer Res; 76(22); 6543-54. ©2016 AACR. |Adenocarcinoma/*genetics/pathology [MESH] |Animals [MESH] |Carcinoma, Pancreatic Ductal/*genetics/pathology [MESH] |Epithelial-Mesenchymal Transition/genetics [MESH] |Female [MESH] |Humans [MESH] |Insulin-Like Growth Factor Binding Protein 2/*metabolism [MESH] |Mice [MESH] |Mice, Nude [MESH] |NF-kappa B/*metabolism [MESH]IGFBP2 Activates the NF-?B Pathway to Drive Epithelial-Mesenchymal Tra(epmc).pdf DeepDyve Pubget Overpricing