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10.1097/CAD.0000000000000585 http://scihub22266oqcxt.onion/10.1097/CAD.0000000000000585 C5821477!5821477 !29360662     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29360662 &cmd=llinks): Failed to open stream: HTTP request failed! 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FoxM1 promotes epithelial-mesenchymal transition, invasion, and migration of tongue squamous cell carcinoma cells through a c-Met/AKT-dependent positive feedback loop |pdf=|usr=}}{{29360662 }} gab.com Text FoxM1 promotes epithelial-mesenchymal transition, invasion, and migration of tongue squamous cell carcinoma cells through a c-Met/AKT-dependent positive feedback loop JO: Anticancer Drugs http://www.kidney.de/pget.php?&tw=1&pmid=29360662 #FOAvip Forkhead box protein M1 (FoxM1) has been associated with cancer progression and metastasis. However, the function of FoxM1 in tongue squamous cell carcinoma (TSCC) remains largely unknown. The purpose of this study was to determine the role of FoxM1 in regulation of epithelial-mesenchymal transition (EMT) and migration of TSCC cells. We found that FoxM1 induced EMT and increased invasion/migration capacity in SCC9 and SCC25 cells. FoxM1 stimulation increased c-Met, pAKT, and vimentin levels but decreased E-cadherin level. Chromatin immunoprecipitation assay established that FoxM1 is bound to the promoter of c-Met to activate its transcription. In turn, c-Met promoted the expression of FoxM1 and pAKT. Blocking AKT signaling attenuated the invasion and migration of SCC9 and SCC25 cells stimulated by FoxM1 or c-Met. These results indicate that a positive feedback loop controls the EMT and migration of TSCC cells induced by FoxM1 and c-Met through AKT. Furthermore, the expression levels of FoxM1, pAKT, and c-Met were found to significantly increase in TSCC tissues compared with normal tissues, and these three biomarkers were concomitantly expressed in TSCC tissues. Clinical association analyses indicated that the expression of FoxM1, c-Met, and pAKT was associated with clinicopathological characteristics of patients with TSCC including tumor stage, tumor size, and lymph node metastasis. Taken together, our findings suggest that FoxM1 promotes the EMT, invasion and migration of TSCC cells, and cross-talks with c-Met/AKT signaling to form a positive feedback loop to promote TSCC development. Twit Text FOAVip FoxM1 promotes epithelial-mesenchymal transition, invasion, and migration of tongue squamous cell carcinoma cells through a c-Met/AKT-dependent positive feedback loop ????Anticancer Drugs http://www.kidney.de/pget.php?&tw=1&pmid=29360662 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29360662 #FOAvip English Wikipedia <ref>{{Cite pmid|29360662 }}</ref> FoxM1 promotes epithelial-mesenchymal transition, invasion, and migration of tongue squamous cell carcinoma cells through a c-Met/AKT-dependent positive feedback loop #MMPMID29360662 Yang H ; Wen L ; Wen M ; Liu T ; Zhao L ; Wu B ; Yun Y ; Liu W ; Wang H ; Wang Y ; Wen N Anticancer Drugs 2018[Mar]; 29 (3 ): 216-226 PMID29360662 show ga Forkhead box protein M1 (FoxM1) has been associated with cancer progression and metastasis. However, the function of FoxM1 in tongue squamous cell carcinoma (TSCC) remains largely unknown. The purpose of this study was to determine the role of FoxM1 in regulation of epithelial-mesenchymal transition (EMT) and migration of TSCC cells. We found that FoxM1 induced EMT and increased invasion/migration capacity in SCC9 and SCC25 cells. FoxM1 stimulation increased c-Met, pAKT, and vimentin levels but decreased E-cadherin level. Chromatin immunoprecipitation assay established that FoxM1 is bound to the promoter of c-Met to activate its transcription. In turn, c-Met promoted the expression of FoxM1 and pAKT. Blocking AKT signaling attenuated the invasion and migration of SCC9 and SCC25 cells stimulated by FoxM1 or c-Met. These results indicate that a positive feedback loop controls the EMT and migration of TSCC cells induced by FoxM1 and c-Met through AKT. Furthermore, the expression levels of FoxM1, pAKT, and c-Met were found to significantly increase in TSCC tissues compared with normal tissues, and these three biomarkers were concomitantly expressed in TSCC tissues. Clinical association analyses indicated that the expression of FoxM1, c-Met, and pAKT was associated with clinicopathological characteristics of patients with TSCC including tumor stage, tumor size, and lymph node metastasis. Taken together, our findings suggest that FoxM1 promotes the EMT, invasion and migration of TSCC cells, and cross-talks with c-Met/AKT signaling to form a positive feedback loop to promote TSCC development. |Carcinoma, Squamous Cell/genetics/*metabolism/pathology [MESH] |Cell Line, Tumor [MESH] |Cell Movement/*physiology [MESH] |Epithelial-Mesenchymal Transition [MESH] |Feedback, Physiological [MESH] |Forkhead Box Protein M1/*metabolism [MESH] |Head and Neck Neoplasms/genetics/*metabolism/pathology [MESH] |Humans [MESH] |Neoplasm Invasiveness [MESH] |Proto-Oncogene Proteins c-akt/*metabolism [MESH] |Proto-Oncogene Proteins c-met/genetics/*metabolism [MESH] |Signal Transduction [MESH] |Squamous Cell Carcinoma of Head and Neck [MESH]FoxM1 promotes epithelial-mesenchymal transition, invasion, and migrat(epmc).pdf DeepDyve Pubget Overpricing