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10.1128/MCB.00373-16 http://scihub22266oqcxt.onion/10.1128/MCB.00373-16 C5021378!5021378 !27402864     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27402864 &cmd=llinks): Failed to open stream: HTTP request failed! 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Mesenchymal-Epithelial Transition in Sarcomas Is Controlled by the Combinatorial Expression of MicroRNA 200s and GRHL2 |pdf=|usr=}}{{27402864 }} gab.com Text Mesenchymal-Epithelial Transition in Sarcomas Is Controlled by the Combinatorial Expression of MicroRNA 200s and GRHL2 JO: Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27402864 #FOAvip Phenotypic plasticity involves a process in which cells transiently acquire phenotypic traits of another lineage. Two commonly studied types of phenotypic plasticity are epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET). In carcinomas, EMT drives invasion and metastatic dissemination, while MET is proposed to play a role in metastatic colonization. Phenotypic plasticity in sarcomas is not well studied; however, there is evidence that a subset of sarcomas undergo an MET-like phenomenon. While the exact mechanisms by which these transitions occur remain largely unknown, it is likely that some of the same master regulators that drive EMT and MET in carcinomas also act in sarcomas. In this study, we combined mathematical models with bench experiments to identify a core regulatory circuit that controls MET in sarcomas. This circuit comprises the microRNA 200 (miR-200) family, ZEB1, and GRHL2. Interestingly, combined expression of miR-200s and GRHL2 further upregulates epithelial genes to induce MET. This effect is phenocopied by downregulation of either ZEB1 or the ZEB1 cofactor, BRG1. In addition, an MET gene expression signature is prognostic for improved overall survival in sarcoma patients. Together, our results suggest that a miR-200, ZEB1, GRHL2 gene regulatory network may drive sarcoma cells to a more epithelial-like state and that this likely has prognostic relevance. Twit Text FOAVip Mesenchymal-Epithelial Transition in Sarcomas Is Controlled by the Combinatorial Expression of MicroRNA 200s and GRHL2 ????Mol Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27402864 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27402864 #FOAvip English Wikipedia <ref>{{Cite pmid|27402864 }}</ref> Mesenchymal-Epithelial Transition in Sarcomas Is Controlled by the Combinatorial Expression of MicroRNA 200s and GRHL2 #MMPMID27402864 Somarelli JA ; Shetler S ; Jolly MK ; Wang X ; Bartholf Dewitt S ; Hish AJ ; Gilja S ; Eward WC ; Ware KE ; Levine H ; Armstrong AJ ; Garcia-Blanco MA Mol Cell Biol 2016[Oct]; 36 (19 ): 2503-13 PMID27402864 show ga Phenotypic plasticity involves a process in which cells transiently acquire phenotypic traits of another lineage. Two commonly studied types of phenotypic plasticity are epithelial-mesenchymal transition (EMT) and mesenchymal-epithelial transition (MET). In carcinomas, EMT drives invasion and metastatic dissemination, while MET is proposed to play a role in metastatic colonization. Phenotypic plasticity in sarcomas is not well studied; however, there is evidence that a subset of sarcomas undergo an MET-like phenomenon. While the exact mechanisms by which these transitions occur remain largely unknown, it is likely that some of the same master regulators that drive EMT and MET in carcinomas also act in sarcomas. In this study, we combined mathematical models with bench experiments to identify a core regulatory circuit that controls MET in sarcomas. This circuit comprises the microRNA 200 (miR-200) family, ZEB1, and GRHL2. Interestingly, combined expression of miR-200s and GRHL2 further upregulates epithelial genes to induce MET. This effect is phenocopied by downregulation of either ZEB1 or the ZEB1 cofactor, BRG1. In addition, an MET gene expression signature is prognostic for improved overall survival in sarcoma patients. Together, our results suggest that a miR-200, ZEB1, GRHL2 gene regulatory network may drive sarcoma cells to a more epithelial-like state and that this likely has prognostic relevance. |*Epithelial-Mesenchymal Transition [MESH] |DNA-Binding Proteins/*genetics [MESH] |Down-Regulation [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Humans [MESH] |MicroRNAs/*genetics [MESH] |Models, Theoretical [MESH] |Neoplasm Invasiveness [MESH] |Neoplasm Metastasis [MESH] |Prognosis [MESH] |Sarcoma/genetics/*pathology [MESH] |Survival Analysis [MESH] |Transcription Factors/*genetics [MESH] |Up-Regulation [MESH]Mesenchymal-Epithelial Transition in Sarcomas Is Controlled by the Com(epmc).pdf DeepDyve Pubget Overpricing