| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 8726268 | Gastroenterology | 2018 | 39 Pages |
Abstract
Expression of MAFG increases in cells and tissues with cholestasis, as well as in human cholangiocarcinoma and HCC specimens; high expression levels correlate with tumor progression and reduced survival time. SAMe and UDCA reduce expression of MAFG in response to cholestasis, by shared and distinct mechanisms. OCA induces MAFG expression, cancer cell proliferation, and growth of xenograft tumors in mice.
Keywords
NF-κBProhibitin 1MAFGUDCATCGAFXROCAAP-1BDLCCAGSHmRNAfarnesoid X receptorHCCmessenger RNASmall interfering RNAsiRNALCAS-adenosylmethionineobeticholic acidLithocholic acidThe cancer genome atlasUrsodeoxycholic acidBrdUantioxidant response elementNuclear factor–κBMatmethionine adenosyltransferasewild typeAREactivator protein-1bile duct ligationHepatocellular carcinomareduced glutathioneCholangiocarcinomaSAMe
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Authors
Ting Liu, Heping Yang, Wei Fan, Jian Tu, Tony W.H. Li, Jiaohong Wang, Hong Shen, JinWon Yang, Ting Xiong, Justin Steggerda, Zhenqiu Liu, Mazen Noureddin, Stephanie S. Maldonado, Alagappan Annamalai, Ekihiro Seki, José M. Mato, Shelly C. Lu,