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10.1016/j.bbrc.2015.08.071 http://scihub22266oqcxt.onion/10.1016/j.bbrc.2015.08.071 26297948!ä!26297948 Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26297948&cmd=llinks): Failed to open stream: HTTP request failed! 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Identification of a PEAK1/ZEB1 signaling axis during TGFbeta/fibronectin-induced EMT in breast cancer |pdf=|usr=}}{{26297948}} gab.com Text Identification of a PEAK1/ZEB1 signaling axis during TGFbeta/fibronectin-induced EMT in breast cancer JO: Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=26297948 #FOAvip Transforming Growth Factor beta (TGFbeta) is the archetypal member of the TGFbeta superfamily of ligands and has pleiotropic functions during normal development, adult tissue homeostasis and pathophysiological processes such as cancer. In epithelial cancers TGFbeta signaling can either suppress tumor growth or promote metastasis via the induction of a well-characterized epithelial-mesenchymal transition (EMT) program. We recently reported that PEAK1 kinase mediates signaling cross talk between TGFbeta receptors and integrin/Src/MAPK pathways and functions as a critical molecular regulator of TGFbeta-induced breast cancer cell proliferation, migration, EMT and metastasis. Here, we examined the breast cancer cell contexts in which TGFbeta induces both EMT and PEAK1, and discovered this event to be unique to oncogene-transformed mammary epithelial cells and triple-negative breast cancer cells. Using the Cancer BioPortal database, we identified PEAK1 co-expressors across multiple malignancies that are also common to the TGFbeta response gene signature (TBRS). We then used the ScanSite database to identify predicted protein-protein binding partners of PEAK1 and the PEAK1-TBRS co-expressors. Analysis of the Cytoscape interactome and Babelomics-derived gene ontologies for a novel gene set including PEAK1, CRK, ZEB1, IL11 and COL4A1 enabled us to hypothesize that PEAK1 may be regulating TGFbeta-induced EMT via its interaction with or regulation of these other genes. In this regard, we have demonstrated that PEAK1 is necessary for TGFbeta to induce ZEB1-mediated EMT in the context of fibronectin/ITGB3 activation. These studies and future mechanistic studies will pave the way toward identifying the context in which TGFbeta blockade may significantly improve breast cancer patient outcomes. Twit Text FOAVip Identification of a PEAK1/ZEB1 signaling axis during TGFbeta/fibronectin-induced EMT in breast cancer ????Biochem Biophys Res Commun http://www.kidney.de/pget.php?&tw=1&pmid=26297948 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26297948 #FOAvip English Wikipedia <ref>{{Cite pmid|26297948}}</ref> Identification of a PEAK1/ZEB1 signaling axis during TGFbeta/fibronectin-induced EMT in breast cancer #MMPMID26297948 Agajanian M; Runa F; Kelber JA Biochem Biophys Res Commun 2015[Sep]; 465 (3): 606-12 PMID26297948show ga Transforming Growth Factor beta (TGFbeta) is the archetypal member of the TGFbeta superfamily of ligands and has pleiotropic functions during normal development, adult tissue homeostasis and pathophysiological processes such as cancer. In epithelial cancers TGFbeta signaling can either suppress tumor growth or promote metastasis via the induction of a well-characterized epithelial-mesenchymal transition (EMT) program. We recently reported that PEAK1 kinase mediates signaling cross talk between TGFbeta receptors and integrin/Src/MAPK pathways and functions as a critical molecular regulator of TGFbeta-induced breast cancer cell proliferation, migration, EMT and metastasis. Here, we examined the breast cancer cell contexts in which TGFbeta induces both EMT and PEAK1, and discovered this event to be unique to oncogene-transformed mammary epithelial cells and triple-negative breast cancer cells. Using the Cancer BioPortal database, we identified PEAK1 co-expressors across multiple malignancies that are also common to the TGFbeta response gene signature (TBRS). We then used the ScanSite database to identify predicted protein-protein binding partners of PEAK1 and the PEAK1-TBRS co-expressors. Analysis of the Cytoscape interactome and Babelomics-derived gene ontologies for a novel gene set including PEAK1, CRK, ZEB1, IL11 and COL4A1 enabled us to hypothesize that PEAK1 may be regulating TGFbeta-induced EMT via its interaction with or regulation of these other genes. In this regard, we have demonstrated that PEAK1 is necessary for TGFbeta to induce ZEB1-mediated EMT in the context of fibronectin/ITGB3 activation. These studies and future mechanistic studies will pave the way toward identifying the context in which TGFbeta blockade may significantly improve breast cancer patient outcomes. |*Epithelial-Mesenchymal Transition[MESH] |Breast Neoplasms/*metabolism[MESH] |Cell Line, Tumor[MESH] |Female[MESH] |Fibronectins/*metabolism[MESH] |Homeodomain Proteins/*metabolism[MESH] |Humans[MESH] |Protein-Tyrosine Kinases/*metabolism[MESH] |Signal Transduction[MESH] |Transcription Factors/*metabolism[MESH] |Transforming Growth Factor beta/*metabolism[MESH]Identification of a PEAK1/ZEB1 signaling axis during TGFbeta/fibronect(epmc).pdf DeepDyve Pubget Overpricing