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10.1038/cddis.2017.111 http://scihub22266oqcxt.onion/10.1038/cddis.2017.111 C5386518!5386518 !28300833     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28300833 &cmd=llinks): Failed to open stream: HTTP request failed! 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PI3K/AKT-mediated upregulation of WDR5 promotes colorectal cancer metastasis by directly targeting ZNF407 |pdf=|usr=}}{{28300833 }} gab.com Text PI3K/AKT-mediated upregulation of WDR5 promotes colorectal cancer metastasis by directly targeting ZNF407 JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28300833 #FOAvip Colorectal cancer (CRC) is the third most common cause of cancer deaths, and has a high rate of liver and lung metastasis. Unfortunately, distant metastasis is the main barrier for advanced CRC therapy and leads to a very low survival rate. In this study, we identified WDR5, a vital factor that regulates vertebrate development and cell self-renewal and reprogramming, as a novel prognostic marker and therapeutic target for CRC patients. We demonstrate that WDR5 is upregulated in CRC tissues and promotes CRC metastasis both in vitro and in vivo. In an effort to investigate the impact of WDR5 on CRC cell fate, we treated CRC cells with growth factor and inhibitor. We report that WDR5 is a novel factor in the metastasis of CRC by triggering epithelial-mesenchymal transition (EMT) process in response to the PI3K/AKT signaling pathway. Moreover, WDR5 shows a direct binding to the ZNF407 promoter on regulating cellular EMT process, leading to CRC metastasis. Hence, our findings strongly position WDR5 as a valuable marker for CRC, and inhibiting WDR5 or the associated signaling pathways may be an effective strategy for the future development of anti-CRC therapy. Twit Text FOAVip PI3K/AKT-mediated upregulation of WDR5 promotes colorectal cancer metastasis by directly targeting ZNF407 ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28300833 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28300833 #FOAvip English Wikipedia <ref>{{Cite pmid|28300833 }}</ref> PI3K/AKT-mediated upregulation of WDR5 promotes colorectal cancer metastasis by directly targeting ZNF407 #MMPMID28300833 Tan X ; Chen S ; Wu J ; Lin J ; Pan C ; Ying X ; Pan Z ; Qiu L ; Liu R ; Geng R ; Huang W Cell Death Dis 2017[Mar]; 8 (3 ): e2686 PMID28300833 show ga Colorectal cancer (CRC) is the third most common cause of cancer deaths, and has a high rate of liver and lung metastasis. Unfortunately, distant metastasis is the main barrier for advanced CRC therapy and leads to a very low survival rate. In this study, we identified WDR5, a vital factor that regulates vertebrate development and cell self-renewal and reprogramming, as a novel prognostic marker and therapeutic target for CRC patients. We demonstrate that WDR5 is upregulated in CRC tissues and promotes CRC metastasis both in vitro and in vivo. In an effort to investigate the impact of WDR5 on CRC cell fate, we treated CRC cells with growth factor and inhibitor. We report that WDR5 is a novel factor in the metastasis of CRC by triggering epithelial-mesenchymal transition (EMT) process in response to the PI3K/AKT signaling pathway. Moreover, WDR5 shows a direct binding to the ZNF407 promoter on regulating cellular EMT process, leading to CRC metastasis. Hence, our findings strongly position WDR5 as a valuable marker for CRC, and inhibiting WDR5 or the associated signaling pathways may be an effective strategy for the future development of anti-CRC therapy. |Biomarkers, Tumor/metabolism [MESH] |Cell Line [MESH] |Cell Line, Tumor [MESH] |Cell Movement/physiology [MESH] |Colorectal Neoplasms/*metabolism/*pathology [MESH] |DNA-Binding Proteins/*metabolism [MESH] |Epithelial-Mesenchymal Transition/physiology [MESH] |Gene Expression Regulation, Neoplastic/physiology [MESH] |HCT116 Cells [MESH] |HEK293 Cells [MESH] |HT29 Cells [MESH] |Histone-Lysine N-Methyltransferase/*metabolism [MESH] |Humans [MESH] |Intracellular Signaling Peptides and Proteins [MESH] |Neoplasm Metastasis/*pathology [MESH] |Phosphatidylinositol 3-Kinases/*metabolism [MESH] |Prognosis [MESH] |Promoter Regions, Genetic/physiology [MESH] |Proto-Oncogene Proteins c-akt/*metabolism [MESH] |Signal Transduction/physiology [MESH] |Transcription Factors/*metabolism [MESH]PI3K/AKT-mediated upregulation of WDR5 promotes colorectal cancer meta(epmc).pdf DeepDyve Pubget Overpricing