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10.3892/ol.2018.8441

http://scihub22266oqcxt.onion/10.3892/ol.2018.8441
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C5958710!5958710!29805610
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suck abstract from ncbi


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pmid29805610      Oncol+Lett 2018 ; 15 (6): 8723-8
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  • Transforming growth factor-? decreases side population cells in hepatocellular carcinoma in vitro #MMPMID29805610
  • Kim JB; Lee S; Kim HR; Park SY; Lee M; Yoon JH; Kim YJ
  • Oncol Lett 2018[Jun]; 15 (6): 8723-8 PMID29805610show ga
  • Hepatocellular carcinoma (HCC) can result from hepatitis B or C infection, fibrosis or cirrhosis. Transforming growth factor-? (TGF-?) is one of the main growth factors associated with fibrosis or cirrhosis progression in the liver, but its role is controversial in hepatocarcinogenesis. In the present study, the effect of TGF-? on the HCC Huh-7 and Huh-Bat cell lines was evaluated. To study the effect of TGF-?, Huh-7 and Huh-Bat cells were treated with TGF-? and a TGF-? receptor inhibitor (SB431542). Cell survival, cell cycle, numbers of side population (SP) cells and expression of the cancer stem cell marker cluster of differentiation (CD)133, epithelial-mesenchymal transition markers (E-cadherin, ?-smooth muscle actin and vimentin) and TGF-?-regulated proteins [phospho-c-Jun N-terminal kinase (p-JNK), p-c-Jun and p-smad2] were investigated. TGF-? treatment resulted in decreased cell survival with a targeted effect on SP cells. Expression of CD133 and vimentin was upregulated by treatment with the TGF-? receptor antagonist SB431542, but not with TGF-?. By contrast, TGF-? induced accumulation of cells at G0/G1, and upregulated expression of p-JNK, p-c-Jun and p-smad2. However, these effects were blocked when cells were treated with TGF-? plus SB431542, indicating the specificity of the TGF-? effect. The present results indicated that TGF-? has anticancer effects mediated by survival inhibition of cancer stem cells, which may be developed as a novel therapy for HCC.
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