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ACOT12-Dependent Alteration of Acetyl-CoA Drives Hepatocellular Carcinoma Metastasis by Epigenetic Induction of Epithelial-Mesenchymal Transition.

Abstract：

:Metabolic reprogramming plays an important role in supporting tumor growth. However, little is known about the metabolic alterations that promote cancer metastasis. In this study, we identify acyl-CoA thioesterase 12 (ACOT12) as a key player in hepatocellular carcinoma (HCC) metastasis. The expression of ACOT12 is significantly down-regulated in HCC tissues and is closely associated with HCC metastasis and poor survival of HCC patients. Gain- and loss-of-function studies demonstrate that ACOT12 suppresses HCC metastasis both in vitro and in vivo. Further mechanistic studies reveal that ACOT12 regulates the cellular acetyl-CoA levels and histone acetylation in HCC cells and that down-regulation of ACOT12 promotes HCC metastasis by epigenetically inducing TWIST2 expression and the promotion of epithelial-mesenchymal transition. Taken together, our findings link the alteration of acetyl-CoA with HCC metastasis and imply that ACOT12 could be a prognostic marker and a potential therapeutic target for combating HCC metastasis.

journal_name

Cell Metab

journal_title

Cell metabolism

authors

Lu M,Zhu WW,Wang X,Tang JJ,Zhang KL,Yu GY,Shao WQ,Lin ZF,Wang SH,Lu L,Zhou J,Wang LX,Jia HL,Dong QZ,Chen JH,Lu JQ,Qin LX

doi

10.1016/j.cmet.2018.12.019

subject

Has Abstract

pub_date

2019-04-02 00:00:00

pages

886-900.e5

issue

4

eissn

1550-4131

issn

1932-7420

pii

S1550-4131(18)30756-3

journal_volume

29

pub_type

杂志文章

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