KAT8 acetylation-controlled lipolysis affects the invasive and migratory potential of colorectal cancer cells

Author:

Qiu Bingquan,Li Shen,Li Meiting,Wang Shuo,Mu Guanqun,Chen Keyu,Wang Meng,Zhu Wei-guo,Wang Weibin,Wang Jiadong,Li Ziyu,Yang JichunORCID,Yang YangORCID

Abstract

AbstractEpigenetic mechanisms involved in gene expression play an essential role in various cellular processes, including lipid metabolism. Lysine acetyltransferase 8 (KAT8), a histone acetyltransferase, has been reported to mediate de novo lipogenesis by acetylating fatty acid synthase. However, the effect of KAT8 on lipolysis is unclear. Here, we report a novel mechanism of KAT8 on lipolysis involving in its acetylation by general control non-repressed protein 5 (GCN5) and its deacetylation by Sirtuin 6 (SIRT6). KAT8 acetylation at K168/175 residues attenuates the binding activity of KAT8 and inhibits the recruitment of RNA pol II to the promoter region of the lipolysis-related genes adipose triglyceride lipase (ATGL) and hormone-sensitive lipase (HSL), subsequently down-regulating lipolysis to affect the invasive and migratory potential of colorectal cancer cells. Our findings uncover a novel mechanism that KAT8 acetylation-controlled lipolysis affects invasive and migratory potential in colorectal cancer cells.

Funder

Natural Science Foundation of Beijing Municipality

National Natural Science Foundation of China

Publisher

Springer Science and Business Media LLC

Subject

Cancer Research,Cell Biology,Cellular and Molecular Neuroscience,Immunology

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