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10.18632/oncotarget.10831 http://scihub22266oqcxt.onion/10.18632/oncotarget.10831 C5312338!5312338!27487122     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27487122&cmd=llinks): Failed to open stream: HTTP request failed! 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Interleukin-11 promotes epithelial-mesenchymal transition in anaplastic thyroid carcinoma cells through PI3K/Akt/GSK3? signaling pathway activation |pdf=|usr=}}{{27487122}} gab.com Text Interleukin-11 promotes epithelial-mesenchymal transition in anaplastic thyroid carcinoma cells through PI3K/Akt/GSK3 signaling pathway activation JO: Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27487122 #FOAvip Metastasis is the major cause of treatment failure in anaplastic thyroid carcinoma (ATC) patients. In the preliminary study, we demonstrated that interleukin (IL)-11 expression is positively correlated with distant metastasis in ATC. However, the mechanisms underlying remain largely unknown. Here, we found that cobalt chloride (a hypoxia mimetic) promoted IL-11 expression via HIF-1? activation. Furthermore, the resultant increase in IL-11 expression significantly induced epithelial-mesenchymal transition (EMT) in ATC cells, accompanied by Akt/GSK3? pathway activation and increased invasive and migratory abilities. Conversely, HIF-1? or IL-11 knockdown, or treating cells with a neutralizing antibody against IL-11, a PI3K inhibitor, or Akt inhibitor V, significantly suppressed the induction of EMT and counteracted the enhancements in invasive and migratory abilities. These results indicate that hypoxia increases IL-11 secretion in ATC cells via HIF-1? induction and that IL-11 then induces EMT in these cells via the PI3K/Akt/GSK3? pathway, ultimately improving their invasive and migratory potential. This study elucidates the prometastatic role played by IL-11 in ATC metastasis and indicates it as a potential target for the treatment of cancer metastasis. However, many questions remain to be explored. Twit Text FOAVip Interleukin-11 promotes epithelial-mesenchymal transition in anaplastic thyroid carcinoma cells through PI3K/Akt/GSK3 signaling pathway activation ????Oncotarget http://www.kidney.de/pget.php?&tw=1&pmid=27487122 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27487122 #FOAvip English Wikipedia <ref>{{Cite pmid|27487122}}</ref> Interleukin-11 promotes epithelial-mesenchymal transition in anaplastic thyroid carcinoma cells through PI3K/Akt/GSK3? signaling pathway activation #MMPMID27487122 Zhong Z; Hu Z; Jiang Y; Sun R; Chen X; Chu H; Zeng M; Sun C Oncotarget 2016[Sep]; 7 (37): 59652-63 PMID27487122show ga Metastasis is the major cause of treatment failure in anaplastic thyroid carcinoma (ATC) patients. In the preliminary study, we demonstrated that interleukin (IL)-11 expression is positively correlated with distant metastasis in ATC. However, the mechanisms underlying remain largely unknown. Here, we found that cobalt chloride (a hypoxia mimetic) promoted IL-11 expression via HIF-1? activation. Furthermore, the resultant increase in IL-11 expression significantly induced epithelial-mesenchymal transition (EMT) in ATC cells, accompanied by Akt/GSK3? pathway activation and increased invasive and migratory abilities. Conversely, HIF-1? or IL-11 knockdown, or treating cells with a neutralizing antibody against IL-11, a PI3K inhibitor, or Akt inhibitor V, significantly suppressed the induction of EMT and counteracted the enhancements in invasive and migratory abilities. These results indicate that hypoxia increases IL-11 secretion in ATC cells via HIF-1? induction and that IL-11 then induces EMT in these cells via the PI3K/Akt/GSK3? pathway, ultimately improving their invasive and migratory potential. This study elucidates the prometastatic role played by IL-11 in ATC metastasis and indicates it as a potential target for the treatment of cancer metastasis. However, many questions remain to be explored. äInterleukin-11 promotes epithelial-mesenchymal transition in anaplasti(epmc).pdf DeepDyve Pubget Overpricing