期刊
BMB REPORTS
卷 50, 期 12, 页码 599-600出版社
KOREAN SOCIETY BIOCHEMISTRY & MOLECULAR BIOLOGY
DOI: 10.5483/BMBRep.2017.50.12.201
关键词
Cancer model; Hepatocellular carcinoma; Snail; Transforming growth factor beta (TGF-beta); Tumor promotion
资金
- National Research Foundation of Korea (NRF) - Korea government (MSIP) [2016R1A2B4013891]
- National Research Foundation of Korea [2016R1A2B4013891] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
Many studies have focused on the tumor suppressive role of TGF-beta signaling during the early stages of tumorigenesis by activating the target genes involved in cytostasis and apoptosis. We investigated the effects of TGF-beta inhibition on early tumorigenesis in the liver, by employing diverse inhibitory methods. Strikingly, TGF-beta inhibition consistently suppressed hepatic tumorigenesis that was induced either by activated RAS plus p53 downregulation or by the co-activation of RAS and TAZ signaling; this demonstrates the requirements for canonical TGF-beta signaling in tumorigenesis. Moreover, we found that Snail is the target gene of the TGF-beta signaling pathway that promotes hepatic carcinogenesis. The knockdown of Snail suppressed the early tumorigenesis in the liver, as did the TGF-beta inhibition, while the ectopic expression of Snail restored tumorigenesis that was suppressed by the TGF-beta inhibition. Our findings establish the oncogenic TGF-beta -Smad-Snail signaling axis during the early tumorigenesis in the liver.
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