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10.18632/oncotarget.13152 http://scihub22266oqcxt.onion/10.18632/oncotarget.13152 C5354848!5354848 !27835861     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27835861 &cmd=llinks): Failed to open stream: HTTP request failed! 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An oncogenic KRAS transcription program activates the RHOGEF ARHGEF2 to mediate transformed phenotypes in pancreatic cancer |pdf=|usr=}}{{27835861 }} gab.com Text An oncogenic KRAS transcription program activates the RHOGEF ARHGEF2 to mediate transformed phenotypes in pancreatic cancer JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27835861 #FOAvip Activating mutations of KRAS are nearly ubiquitous in pancreatic adenocarcinomas occurring in greater than 90% of cases. Cellular transformation by oncogenic RAS requires the RHO guanine exchange factor ARHGEF2 (also known as GEF-H1) for tumor growth and survival. Here, we find oncogenic KRAS activates ARHGEF2 through a minimal RAS responsive promoter. We have determined the endogenous ARHGEF2 promoter is positively regulated by the transcription factors ELK1, ETS1, SP1 and SP3 and negatively regulated by the RAS responsive element binding protein (RREB1). We find that the panel of ARHGEF2-regulating transcription factors modulates RAS transformed phenotypes including cellular viability, anchorage-independent growth and invasion-migration of pancreatic cancer cells. RREB1 knockdown activates the amplitude and duration of RHOA via increased ARHGEF2 expression. By relieving the negative regulation of RREB1 on the ARHGEF2 promoter, we determined that ETS1 and SP3 are essential for the normal expression of ARHGEF2 and contribute to the migratory behavior of pancreatic cancer cells. Furthermore, enforced expression of ARHGEF2 rescues loss of SP3 driven invasion-migration and anchorage-independent growth defective phenotypes through restored activation of RHOA. Collectively, our results identify a transcription factor program required for RAS transformation and provide mechanistic insight into the highly metastatic behavior of pancreatic cancer. Twit Text FOAVip An oncogenic KRAS transcription program activates the RHOGEF ARHGEF2 to mediate transformed phenotypes in pancreatic cancer ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27835861 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27835861 #FOAvip English Wikipedia <ref>{{Cite pmid|27835861 }}</ref> An oncogenic KRAS transcription program activates the RHOGEF ARHGEF2 to mediate transformed phenotypes in pancreatic cancer #MMPMID27835861 Kent OA ; Sandí MJ ; Burston HE ; Brown KR ; Rottapel R Oncotarget 2017[Jan]; 8 (3 ): 4484-4500 PMID27835861 show ga Activating mutations of KRAS are nearly ubiquitous in pancreatic adenocarcinomas occurring in greater than 90% of cases. Cellular transformation by oncogenic RAS requires the RHO guanine exchange factor ARHGEF2 (also known as GEF-H1) for tumor growth and survival. Here, we find oncogenic KRAS activates ARHGEF2 through a minimal RAS responsive promoter. We have determined the endogenous ARHGEF2 promoter is positively regulated by the transcription factors ELK1, ETS1, SP1 and SP3 and negatively regulated by the RAS responsive element binding protein (RREB1). We find that the panel of ARHGEF2-regulating transcription factors modulates RAS transformed phenotypes including cellular viability, anchorage-independent growth and invasion-migration of pancreatic cancer cells. RREB1 knockdown activates the amplitude and duration of RHOA via increased ARHGEF2 expression. By relieving the negative regulation of RREB1 on the ARHGEF2 promoter, we determined that ETS1 and SP3 are essential for the normal expression of ARHGEF2 and contribute to the migratory behavior of pancreatic cancer cells. Furthermore, enforced expression of ARHGEF2 rescues loss of SP3 driven invasion-migration and anchorage-independent growth defective phenotypes through restored activation of RHOA. Collectively, our results identify a transcription factor program required for RAS transformation and provide mechanistic insight into the highly metastatic behavior of pancreatic cancer. |*Transcriptional Activation [MESH] |Cell Line, Tumor [MESH] |Cell Movement [MESH] |Cell Survival [MESH] |Cell Transformation, Neoplastic/*genetics/metabolism [MESH] |DNA-Binding Proteins/metabolism [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Humans [MESH] |Mutation [MESH] |Pancreatic Neoplasms/*genetics/metabolism [MESH] |Phenotype [MESH] |Promoter Regions, Genetic [MESH] |Proto-Oncogene Protein c-ets-1/metabolism [MESH] |Proto-Oncogene Proteins p21(ras)/*genetics/metabolism [MESH] |Rho Guanine Nucleotide Exchange Factors/*genetics [MESH] |Signal Transduction [MESH] |Sp3 Transcription Factor/metabolism [MESH]An oncogenic KRAS transcription program activates the RHOGEF ARHGEF2 t(epmc).pdf DeepDyve Pubget Overpricing