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10.1128/MCB.00510-16 http://scihub22266oqcxt.onion/10.1128/MCB.00510-16 C5335515!5335515 !27956702     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27956702 &cmd=llinks): Failed to open stream: HTTP request failed! 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Snail-Modulated MicroRNA 493 Forms a Negative Feedback Loop with the Insulin-Like Growth Factor 1 Receptor Pathway and Blocks Tumorigenesis |pdf=|usr=}}{{27956702 }} gab.com Text Snail-Modulated MicroRNA 493 Forms a Negative Feedback Loop with the Insulin-Like Growth Factor 1 Receptor Pathway and Blocks Tumorigenesis JO: Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27956702 #FOAvip In this study, we have identified one microRNA, microRNA 493 (miR-493), which could simultaneously and directly regulate multiple genes downstream of the insulin-like growth factor 1 receptor (IGF1R) pathway, including IGF1R, by binding with complementary sequences in the 3' untranslated region (UTR) of mRNAs of IGF1R, insulin receptor substrate 1 (IRS1), and mitogen-activated protein kinase 1 (MAPK1), thereby potentiating their inhibitory function at multiple levels in development and progression of cancers. This binding was further confirmed by pulldown of miR with AGO-2 antibody. Further, results from head and neck samples showed that miR-493 levels were significantly downregulated in tumors, with a concomitant increase in the expression of IGF1R and key downstream effectors. Functional studies from miR-493 overexpression cells and nude-mouse models revealed the tumor suppressor functions of miR-493. Regulation studies revealed that Snail binds to the miR-493 promoter and represses it. We found the existence of a dynamic negative feedback loop in the regulation of IGF1R and miR-493 mediated via Snail. Our study showed that nicotine treatment significantly decreases the levels of miR-493-with a concomitant increase in the levels of Snail-an indication of progression of cells toward tumorigenesis, reestablishing the role of tobacco as a major risk factor for head and neck cancers and elucidating the mechanism behind nicotine-mediated tumorigenesis. Twit Text FOAVip Snail-Modulated MicroRNA 493 Forms a Negative Feedback Loop with the Insulin-Like Growth Factor 1 Receptor Pathway and Blocks Tumorigenesis ????Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27956702 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27956702 #FOAvip English Wikipedia <ref>{{Cite pmid|27956702 }}</ref> Snail-Modulated MicroRNA 493 Forms a Negative Feedback Loop with the Insulin-Like Growth Factor 1 Receptor Pathway and Blocks Tumorigenesis #MMPMID27956702 Kumar AS ; Jagadeeshan S ; Pitani RS ; Ramshankar V ; Venkitasamy K ; Venkatraman G ; Rayala SK Mol Cell Biol 2017[Mar]; 37 (6 ): ä PMID27956702 show ga In this study, we have identified one microRNA, microRNA 493 (miR-493), which could simultaneously and directly regulate multiple genes downstream of the insulin-like growth factor 1 receptor (IGF1R) pathway, including IGF1R, by binding with complementary sequences in the 3' untranslated region (UTR) of mRNAs of IGF1R, insulin receptor substrate 1 (IRS1), and mitogen-activated protein kinase 1 (MAPK1), thereby potentiating their inhibitory function at multiple levels in development and progression of cancers. This binding was further confirmed by pulldown of miR with AGO-2 antibody. Further, results from head and neck samples showed that miR-493 levels were significantly downregulated in tumors, with a concomitant increase in the expression of IGF1R and key downstream effectors. Functional studies from miR-493 overexpression cells and nude-mouse models revealed the tumor suppressor functions of miR-493. Regulation studies revealed that Snail binds to the miR-493 promoter and represses it. We found the existence of a dynamic negative feedback loop in the regulation of IGF1R and miR-493 mediated via Snail. Our study showed that nicotine treatment significantly decreases the levels of miR-493-with a concomitant increase in the levels of Snail-an indication of progression of cells toward tumorigenesis, reestablishing the role of tobacco as a major risk factor for head and neck cancers and elucidating the mechanism behind nicotine-mediated tumorigenesis. |*Feedback, Physiological/drug effects [MESH] |*Signal Transduction/drug effects [MESH] |Animals [MESH] |Binding Sites [MESH] |Carcinogenesis/drug effects/genetics/*pathology [MESH] |Cell Line, Tumor [MESH] |Cell Proliferation/drug effects [MESH] |Down-Regulation/drug effects/genetics [MESH] |Epithelial-Mesenchymal Transition/drug effects [MESH] |Gene Expression Regulation, Neoplastic/drug effects [MESH] |Genes, Tumor Suppressor [MESH] |Head and Neck Neoplasms/genetics/pathology [MESH] |Humans [MESH] |Kinetics [MESH] |Mice, Nude [MESH] |MicroRNAs/genetics/*metabolism [MESH] |Models, Biological [MESH] |Nicotine/pharmacology [MESH] |Receptor, IGF Type 1/*metabolism [MESH] |Snail Family Transcription Factors/genetics/*metabolism [MESH]Snail-Modulated MicroRNA 493 Forms a Negative Feedback Loop with the I(epmc).pdf DeepDyve Pubget Overpricing