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10.1158/0008-5472.CAN-14-0681 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-14-0681 C4359962!4359962!25600647     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 267.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Res 2015 ; 75 (6): 1009-20 Nephropedia Template TP {{tp|p=25600647|t=2015. ?-arrestin-1 mediates nicotine-induced metastasis through E2F1 target genes that modulate epithelial-mesenchymal transition |pdf=|usr=}}{{25600647}} gab.com Text -arrestin-1 mediates nicotine-induced metastasis through E2F1 target genes that modulate epithelial-mesenchymal transition JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25600647 #FOAvip Cigarette smoking is a major risk factor in the development of non-small cell lung cancer (NSCLC), which accounts for 80% of all lung cancers. Nicotine, the major addictive component of tobacco smoke, can induce proliferation, invasion and epithelial-mesenchymal transition (EMT) in NSCLC cell lines and promote metastasis of NSCLC in mice. Here we demonstrate that the scaffolding protein ?-arrestin-1 is necessary for nicotine-mediated induction of mesenchymal genes vimentin and fibronectin as well as EMT regulators ZEB1 and ZEB2. Nicotine induced changes in cell morphology and ablate tight junctions consistent with EMT; ?-arrestin-1, but not ?-arrestin-2, was required for these changes. ?-arrestin-1 promoted the expression of the mesenchymal genes as well as ZEB1 and ZEB2 through the mediation of the E2F1 transcription factor; this required Src kinase activity. Stimulation of multiple NSCLC cell lines with nicotine led to enhanced recruitment of ?-arrestin-1 and E2F1 on vimentin, fibronectin, ZEB1 and ZEB2 promoters. Further, there was significantly more ?-arrestin-1 and E2F1 associated with these promoters in human NSCLC tumors and ?-arrestin-1 levels correlated with vimentin and fibronectin levels in human NSCLC samples. A549-luciferase cells lacking ?-arrestin-1 showed a significantly reduced capacity for tumor growth and metastasis when orthotopically implanted into the lungs of SCID-beige mice. Taken together, these studies reveal a novel role for ?-arrestin-1 in the growth and metastasis of NSCLC. Twit Text FOAVip -arrestin-1 mediates nicotine-induced metastasis through E2F1 target genes that modulate epithelial-mesenchymal transition ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=25600647 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25600647 #FOAvip English Wikipedia <ref>{{Cite pmid|25600647}}</ref> ?-arrestin-1 mediates nicotine-induced metastasis through E2F1 target genes that modulate epithelial-mesenchymal transition #MMPMID25600647 Pillai S; Trevino J; Rawal B; Singh S; Kovacs M; Li X; Schell M; Haura E; Bepler G; Chellappan S Cancer Res 2015[Mar]; 75 (6): 1009-20 PMID25600647show ga Cigarette smoking is a major risk factor in the development of non-small cell lung cancer (NSCLC), which accounts for 80% of all lung cancers. Nicotine, the major addictive component of tobacco smoke, can induce proliferation, invasion and epithelial-mesenchymal transition (EMT) in NSCLC cell lines and promote metastasis of NSCLC in mice. Here we demonstrate that the scaffolding protein ?-arrestin-1 is necessary for nicotine-mediated induction of mesenchymal genes vimentin and fibronectin as well as EMT regulators ZEB1 and ZEB2. Nicotine induced changes in cell morphology and ablate tight junctions consistent with EMT; ?-arrestin-1, but not ?-arrestin-2, was required for these changes. ?-arrestin-1 promoted the expression of the mesenchymal genes as well as ZEB1 and ZEB2 through the mediation of the E2F1 transcription factor; this required Src kinase activity. Stimulation of multiple NSCLC cell lines with nicotine led to enhanced recruitment of ?-arrestin-1 and E2F1 on vimentin, fibronectin, ZEB1 and ZEB2 promoters. Further, there was significantly more ?-arrestin-1 and E2F1 associated with these promoters in human NSCLC tumors and ?-arrestin-1 levels correlated with vimentin and fibronectin levels in human NSCLC samples. A549-luciferase cells lacking ?-arrestin-1 showed a significantly reduced capacity for tumor growth and metastasis when orthotopically implanted into the lungs of SCID-beige mice. Taken together, these studies reveal a novel role for ?-arrestin-1 in the growth and metastasis of NSCLC. ä?-arrestin-1 mediates nicotine-induced metastasis through E2F1 target (epmc).pdf DeepDyve Pubget Overpricing