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As an essential post-translational modification, acetylation participates in various cellular processes and shows aberrances during tumorigenesis. Owing to its modification substrate, acetyl-CoA, acetylation is postulated as a depot for acetyl groups and evolve to build a connection between epigenetics and metabolism. Here we depict a distinct acetylome atlas of hepatocellular carcinoma from the perspectives of both protein acetylation and acetyl-CoA metabolism. We found that tumor acetylome demonstrated a compartment-dependent alteration that the acetylation level of mitochondrial proteins tended to be decreased while nuclear proteins were highly acetylated. In addition, elevated expression of ATP-citrate synthase (ACLY) was observed in tumors, which would facilitate histone acetylation by transporting mitochondrial acetyl coenzyme A to the nucleus. A hypothetical model of the oncogenic acetylome was proposed that growing demands for histone acetylation in tumor cells would drive the relocalization of acetyl-CoA to the nucleus, which may contribute to the global deacetylation of mitochondrial proteins to support the nuclear acetyl-CoA pool in an ACLY-dependent manner. Our findings are thought-provoking on the potential linkage between epigenetics and metabolism in the progression of tumorigenesis. Copyright © 2021. Published by Elsevier B.V.


Xiaowen Hu, Dandan Wang, Liya Sun, Yan Gao, Daizhan Zhou, Xuemei Tong, Jing Li, Hui Lin, Ying Qing, Shujiao Du, Xuhan Yang, Jie Jiang, Guoquan Yan, Zhiyun Wei, Qingyu Wang, Juan Zhang, Lin He, Chunling Wan. Disturbed mitochondrial acetylation in accordance with the availability of acetyl groups in hepatocellular carcinoma. Mitochondrion. 2021 Sep;60:150-159

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PMID: 34375734

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