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10.1158/0008-5472.CAN-13-3182 http://scihub22266oqcxt.onion/10.1158/0008-5472.CAN-13-3182 C4102645!4102645!24830721     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Res 2014 ; 74 (14): 3740-52 Nephropedia Template TP {{tp|p=24830721|t=2014. Autophagy Inhibition by Sustained Over-production of IL-6 Contributes to Arsenic Carcinogenesis |pdf=|usr=}}{{24830721}} gab.com Text Autophagy Inhibition by Sustained Over-production of IL-6 Contributes to Arsenic Carcinogenesis JO: Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24830721 #FOAvip Chronic inflammation has been implicated as an etiological factor in cancer, whereas autophagy may help preserve cancer cell survival but exert anti-inflammatory effects. How these phenomena interact during carcinogenesis remains unclear. We explored this question in a human bronchial epithelial cell-based model of lung carcinogenesis that is mediated by sub-chronic exposure to arsenic. We found that sustained overexpression of the pro-inflammatory interleukin IL-6 promoted arsenic-induced cell transformation by inhibiting autophagy. Conversely, strategies to enhance autophagy counteracted the effect of IL-6 in the model. These findings were confirmed and extended in a mouse model of arsenic-induced lung cancer. Mechanistic investigations suggested that mTOR inhibition contributed to the activation of autophagy, whereas IL-6 overexpression was sufficient to block autophagy by supporting Beclin-1/Mcl-1 interaction. Overall, our findings argued that chronic inflammatory states driven by IL-6 could antagonize autophagic states that may help preserve cancer cell survival and promote malignant progression, suggesting a need to uncouple inflammation and autophagy controls to enable tumor progression. Twit Text FOAVip Autophagy Inhibition by Sustained Over-production of IL-6 Contributes to Arsenic Carcinogenesis ????Cancer Res http://www.kidney.de/pget.php?&tw=1&pmid=24830721 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24830721 #FOAvip English Wikipedia <ref>{{Cite pmid|24830721}}</ref> Autophagy Inhibition by Sustained Over-production of IL-6 Contributes to Arsenic Carcinogenesis #MMPMID24830721 Qi Y; Zhang M; Li H; Frank JA; Dai L; Liu H; Zhang Z; Wang C; Chen G Cancer Res 2014[Jul]; 74 (14): 3740-52 PMID24830721show ga Chronic inflammation has been implicated as an etiological factor in cancer, whereas autophagy may help preserve cancer cell survival but exert anti-inflammatory effects. How these phenomena interact during carcinogenesis remains unclear. We explored this question in a human bronchial epithelial cell-based model of lung carcinogenesis that is mediated by sub-chronic exposure to arsenic. We found that sustained overexpression of the pro-inflammatory interleukin IL-6 promoted arsenic-induced cell transformation by inhibiting autophagy. Conversely, strategies to enhance autophagy counteracted the effect of IL-6 in the model. These findings were confirmed and extended in a mouse model of arsenic-induced lung cancer. Mechanistic investigations suggested that mTOR inhibition contributed to the activation of autophagy, whereas IL-6 overexpression was sufficient to block autophagy by supporting Beclin-1/Mcl-1 interaction. Overall, our findings argued that chronic inflammatory states driven by IL-6 could antagonize autophagic states that may help preserve cancer cell survival and promote malignant progression, suggesting a need to uncouple inflammation and autophagy controls to enable tumor progression. äAutophagy Inhibition by Sustained Over-production of IL-6 Contributes (epmc).pdf DeepDyve Pubget Overpricing