{Reference Type}: Journal Article
{Title}: ACOT12-Dependent Alteration of Acetyl-CoA Drives Hepatocellular Carcinoma Metastasis by Epigenetic Induction of Epithelial-Mesenchymal Transition.
{Author}: 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;
{Journal}: Cell Metab
{Volume}: 29
{Issue}: 4
{Year}: 04 2019 2
{Factor}: 31.373
{DOI}: 10.1016/j.cmet.2018.12.019
{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.