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10.1038/s41419-018-0810-8 http://scihub22266oqcxt.onion/10.1038/s41419-018-0810-8 C6056562!6056562 !30038258     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=30038258 &cmd=llinks): Failed to open stream: HTTP request failed! 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Suppression of Notch1 and AKT mediated epithelial to mesenchymal transition by Verrucarin J in metastatic colon cancer |pdf=|usr=}}{{30038258 }} gab.com Text Suppression of Notch1 and AKT mediated epithelial to mesenchymal transition by Verrucarin J in metastatic colon cancer JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=30038258 #FOAvip Epithelial to mesenchymal transition (EMT) in colorectal cancer (CRC) has been attributed to activation of AKT and Notch1 signaling pathways. As EMT corresponds to increased aggressiveness of CRC, approaches that prevent metastasis by targeting AKT/Notch1 pathways are at the forefront of current research paradigms. This study examined the anti-metastatic potential of Verrucarin J (VJ), a small molecule, in CRC cells overexpressing AKT and Notch1. VJ significantly inhibited AKT/HCT 116 cell growth by acting on the AKT/NF?B/Bcl-2 signaling axis and initiated apoptotic signaling as was evident from increased expression of pro-apoptotic markers such as cleaved PARP, cleaved caspase 3, and cleaved caspase 9. Also, VJ inhibited the cell growth in AKT/Notch1-overexpressing CRC cells and abrogated EMT. The down-regulation of AKT and Notch1 signaling was apparent in immunoblot analysis and corresponded with down-regulation of mesenchymal markers including Snail, and ?-catenin. Intraperitoneal administration of VJ in control (pCMV/HCT 116) and AKT/HCT 116 mice significantly suppressed AKT-induced tumor growth in a xenograft model. In addition, down-regulation of prosurvival markers as well as AKT and Notch1 was observed in the immunohistochemical analysis of the xenografted tumors. In conclusion, our study substantiates the role of AKT and Notch1 in cell proliferation, angiogenesis, and EMT of CRC cells and demonstrates that VJ may be a viable therapeutic option to counter AKT-induced cell proliferation and tumor outgrowth in CRC. Twit Text FOAVip Suppression of Notch1 and AKT mediated epithelial to mesenchymal transition by Verrucarin J in metastatic colon cancer ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=30038258 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30038258 #FOAvip English Wikipedia <ref>{{Cite pmid|30038258 }}</ref> Suppression of Notch1 and AKT mediated epithelial to mesenchymal transition by Verrucarin J in metastatic colon cancer #MMPMID30038258 Pal D ; Tyagi A ; Chandrasekaran B ; Alattasi H ; Ankem MK ; Sharma AK ; Damodaran C Cell Death Dis 2018[Jul]; 9 (8 ): 798 PMID30038258 show ga Epithelial to mesenchymal transition (EMT) in colorectal cancer (CRC) has been attributed to activation of AKT and Notch1 signaling pathways. As EMT corresponds to increased aggressiveness of CRC, approaches that prevent metastasis by targeting AKT/Notch1 pathways are at the forefront of current research paradigms. This study examined the anti-metastatic potential of Verrucarin J (VJ), a small molecule, in CRC cells overexpressing AKT and Notch1. VJ significantly inhibited AKT/HCT 116 cell growth by acting on the AKT/NF?B/Bcl-2 signaling axis and initiated apoptotic signaling as was evident from increased expression of pro-apoptotic markers such as cleaved PARP, cleaved caspase 3, and cleaved caspase 9. Also, VJ inhibited the cell growth in AKT/Notch1-overexpressing CRC cells and abrogated EMT. The down-regulation of AKT and Notch1 signaling was apparent in immunoblot analysis and corresponded with down-regulation of mesenchymal markers including Snail, and ?-catenin. Intraperitoneal administration of VJ in control (pCMV/HCT 116) and AKT/HCT 116 mice significantly suppressed AKT-induced tumor growth in a xenograft model. In addition, down-regulation of prosurvival markers as well as AKT and Notch1 was observed in the immunohistochemical analysis of the xenografted tumors. In conclusion, our study substantiates the role of AKT and Notch1 in cell proliferation, angiogenesis, and EMT of CRC cells and demonstrates that VJ may be a viable therapeutic option to counter AKT-induced cell proliferation and tumor outgrowth in CRC. |Animals [MESH] |Apoptosis/drug effects [MESH] |Cell Line, Tumor [MESH] |Cell Movement [MESH] |Cell Proliferation [MESH] |Colonic Neoplasms/metabolism/pathology [MESH] |Down-Regulation/*drug effects [MESH] |Epithelial-Mesenchymal Transition/*drug effects [MESH] |Humans [MESH] |Mice [MESH] |Mice, Nude [MESH] |Proto-Oncogene Proteins c-akt/genetics/*metabolism [MESH] |Receptor, Notch1/*metabolism [MESH] |Signal Transduction [MESH] |Transplantation, Heterologous [MESH]Suppression of Notch1 and AKT mediated epithelial to mesenchymal trans(epmc).pdf DeepDyve Pubget Overpricing