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10.18632/oncotarget.5035 http://scihub22266oqcxt.onion/10.18632/oncotarget.5035 C4741625!4741625 !26427040     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26427040 &cmd=llinks): Failed to open stream: HTTP request failed! 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Decoding c-Myc networks of cell cycle and apoptosis regulated genes in a transgenic mouse model of papillary lung adenocarcinomas |pdf=|usr=}}{{26427040 }} gab.com Text Decoding c-Myc networks of cell cycle and apoptosis regulated genes in a transgenic mouse model of papillary lung adenocarcinomas JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26427040 #FOAvip The c-Myc gene codes for a basic-helix-loop-helix-leucine zipper transcription factor protein and is reported to be frequently over-expressed in human cancers. Given that c-Myc plays an essential role in neoplastic transformation we wished to define its activity in lung cancer and therefore studied its targeted expression to respiratory epithelium in a transgenic mouse disease model. Using histological well-defined tumors, transcriptome analysis identified novel c-Myc responsive cell cycle and apoptosis genes that were validated as direct c-Myc targets using EMSA, Western blotting, gene reporter and ChIP assays.Through computational analyses c-Myc cooperating transcription factors emerged for repressed and up-regulated genes in cancer samples, namely Klf7, Gata3, Sox18, p53 and Elf5 and Cebp?, respectively. Conversely, at promoters of genes regulated in transgenic but non-carcinomatous lung tissue enriched binding sites for c-Myc, Hbp1, Hif1 were observed. Bioinformatic analysis of tumor transcriptomic data revealed regulatory gene networks and highlighted mortalin and moesin as master regulators while gene reporter and ChIP assays in the H1299 lung cancer cell line as well as cross-examination of published ChIP-sequence data of 7 human and 2 mouse cell lines provided strong evidence for the identified genes to be c-Myc targets. The clinical significance of findings was established by evaluating expression of orthologous proteins in human lung cancer. Taken collectively, a molecular circuit for c-Myc-dependent cellular transformation was identified and the network analysis broadened the perspective for molecularly targeted therapies. Twit Text FOAVip Decoding c-Myc networks of cell cycle and apoptosis regulated genes in a transgenic mouse model of papillary lung adenocarcinomas ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=26427040 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26427040 #FOAvip English Wikipedia <ref>{{Cite pmid|26427040 }}</ref> Decoding c-Myc networks of cell cycle and apoptosis regulated genes in a transgenic mouse model of papillary lung adenocarcinomas #MMPMID26427040 Ciribilli Y ; Singh P ; Spanel R ; Inga A ; Borlak J Oncotarget 2015[Oct]; 6 (31 ): 31569-92 PMID26427040 show ga The c-Myc gene codes for a basic-helix-loop-helix-leucine zipper transcription factor protein and is reported to be frequently over-expressed in human cancers. Given that c-Myc plays an essential role in neoplastic transformation we wished to define its activity in lung cancer and therefore studied its targeted expression to respiratory epithelium in a transgenic mouse disease model. Using histological well-defined tumors, transcriptome analysis identified novel c-Myc responsive cell cycle and apoptosis genes that were validated as direct c-Myc targets using EMSA, Western blotting, gene reporter and ChIP assays.Through computational analyses c-Myc cooperating transcription factors emerged for repressed and up-regulated genes in cancer samples, namely Klf7, Gata3, Sox18, p53 and Elf5 and Cebp?, respectively. Conversely, at promoters of genes regulated in transgenic but non-carcinomatous lung tissue enriched binding sites for c-Myc, Hbp1, Hif1 were observed. Bioinformatic analysis of tumor transcriptomic data revealed regulatory gene networks and highlighted mortalin and moesin as master regulators while gene reporter and ChIP assays in the H1299 lung cancer cell line as well as cross-examination of published ChIP-sequence data of 7 human and 2 mouse cell lines provided strong evidence for the identified genes to be c-Myc targets. The clinical significance of findings was established by evaluating expression of orthologous proteins in human lung cancer. Taken collectively, a molecular circuit for c-Myc-dependent cellular transformation was identified and the network analysis broadened the perspective for molecularly targeted therapies. |*Gene Regulatory Networks [MESH] |Adenocarcinoma of Lung [MESH] |Adenocarcinoma, Papillary/genetics/*metabolism/pathology [MESH] |Adenocarcinoma/*genetics/metabolism/pathology [MESH] |Animals [MESH] |Apoptosis [MESH] |Apoptosis Regulatory Proteins/*genetics/metabolism [MESH] |Binding Sites [MESH] |Blotting, Western [MESH] |Cell Cycle [MESH] |Cell Cycle Proteins/*genetics/metabolism [MESH] |Cell Line, Tumor [MESH] |Chromatin Immunoprecipitation [MESH] |Computational Biology [MESH] |Electrophoretic Mobility Shift Assay [MESH] |Gene Expression Profiling/methods [MESH] |Gene Expression Regulation, Neoplastic [MESH] |Genes, Reporter [MESH] |Genetic Predisposition to Disease [MESH] |Humans [MESH] |Lung Neoplasms/*genetics/metabolism/pathology [MESH] |Mice, Transgenic [MESH] |Phenotype [MESH] |Promoter Regions, Genetic [MESH] |Proto-Oncogene Proteins c-myc/*genetics/metabolism [MESH] |Signal Transduction [MESH]Decoding c-Myc networks of cell cycle and apoptosis regulated genes in(epmc).pdf DeepDyve Pubget Overpricing