Abstract
Many studies have focused on the tumor suppressive role of TGF-β signaling during the early stages of tumorigenesis by activating the target genes involved in cytostasis and apoptosis. We investigated the effects of TGF-β inhibition on early tumorigenesis in the liver, by employing diverse inhibitory methods. Strikingly, TGF-β 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-β signaling in tumorigenesis. Moreover, we found that Snail is the target gene of the TGF-β signaling pathway that promotes hepatic carcinogenesis. The knockdown of Snail suppressed the early tumorigenesis in the liver, as did the TGF-β inhibition, while the ectopic expression of Snail restored tumorigenesis that was suppressed by the TGF-β inhibition. Our findings establish the oncogenic TGF-β-Smad- Snail signaling axis during the early tumorigenesis in the liver.
Original language | English |
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Pages (from-to) | 599-600 |
Number of pages | 2 |
Journal | BMB reports |
Volume | 50 |
Issue number | 12 |
DOIs | |
Publication status | Published - 2017 Dec 1 |
Bibliographical note
Funding Information:This work was supported by the National Research Foundation of Korea (NRF) grant 2016R1A2B4013891 (awarded to S.W.R.), which was funded by the Korea government (MSIP)
Publisher Copyright:
© 2017 by the The Korean Society for Biochemistry and Molecular Biology.
All Science Journal Classification (ASJC) codes
- Biochemistry
- Molecular Biology