Journal
CELL METABOLISM
Volume 29, Issue 4, Pages 886-+Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2018.12.019
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Funding
- State Key Basic Research Program of China [2013CB910500]
- National Key Project for Infectious Disease of China [2012ZX10002012, 2017ZX10203207]
- National Natural Science Foundation of China [81502501, 81472677, 81672820]
- Shanghai Rising-Star Program [17QA140070]
- Research Startup Foundation of Huashan Hospital [2016QD030]
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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 lossof-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.
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