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10.12659/MSM.901542

http://scihub22266oqcxt.onion/10.12659/MSM.901542
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C5417590!5417590!28446743
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suck abstract from ncbi


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pmid28446743      Med+Sci+Monit 2017 ; 23 (ä): 2017-28
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  • Mammalian Target of Rapamycin (mTOR) Regulates Transforming Growth Factor-?1 (TGF-?1)-Induced Epithelial-Mesenchymal Transition via Decreased Pyruvate Kinase M2 (PKM2) Expression in Cervical Cancer Cells #MMPMID28446743
  • Cheng Ky; Hao M
  • Med Sci Monit 2017[]; 23 (ä): 2017-28 PMID28446743show ga
  • Background: Epithelial-mesenchymal transition (EMT) plays an important role in cancer tumorigenesis. Transforming growth factor ?1 (TGF-?1) can induced EMT, which could increase tumor migration and invasion. Moreover, recent studies have been proven that mammalian target of rapamycin (mTOR) is a critical regulator of EMT. We investigated the mechanisms of mTOR in transforming growth factor ?1 (TGF-?1)-induced EMT in cervical cancer cells. Material/Methods: HeLa and SiHa cells were treated with 10 ng/ml TGF-?1 to induce EMT. Then, they were treated with or without rapamycin. CCK8 assay was performed to determine cell proliferation. Cell migration was detected by wound-healing assay; apoptosis was analyzed by flow cytometry; mTOR inhibitors inhibited mTOR pathway to assess the expression of E-cadherin, Vimentin STAT3, Snail2, p-p70s6k, and PKM2 expression. Results: TGF-?1 promoted proliferation and migration, and attenuated apoptosis in cervical carcinoma cells. Rapamycin abolished TGF-?1-induced EMT cell proliferation and migration and reversed TGF-?1-induced EMT. E-cadherin were suppressed, whereas Vimentin and PKM2 were increased in HeLa and SiHa cells after stimulation with TGF-?1. Moreover, mTOR was activated in the process of TGF-?1-induced EMT. Rapamycin inhibited the phosphorylation of p70s6k. Furthermore, inhibition of the mTOR pathway decreased PKM2 expression. Conclusions: Inhibition of the mTOR pathway abolished TGF-?1-induced EMT and reduced mTOR/p70s6k signaling, which downregulated PKM2 expression. Our results provide novel mechanistic insight into the anti-tumor effects of inhibition of mTOR.
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