肝细胞癌
癌症研究
组蛋白
新陈代谢
生物
医学
内科学
生物化学
基因
作者
Wenfei Du,Sheng Tan,Yonglin Peng,Sang Lin,Yunqiang Wu,Keshuo Ding,Changyu Chen,Ruiqi Liu,Yu Cao,Zheyi Li,Sijie Gu,Haoran Feng,Bingbing Wan,Sheng‐ce Tao,Niansong Wang,Ying Fan,Xiaodong Zhao
出处
期刊:Cancer Letters
[Elsevier BV]
日期:2024-12-24
卷期号:611: 217426-217426
被引量:22
标识
DOI:10.1016/j.canlet.2024.217426
摘要
Lipid metabolism reprogramming is critical for the initiation and progression of hepatocellular carcinoma (HCC). However, how the dysregulation of lipid metabolism contributes to HCC development remains largely unknown. Here, we report that the m6A reader YTHDC1-mediated epigenetic regulation of the long noncoding RNA NEAT1 activates stearoyl-CoA desaturase (SCD)-associated lipid metabolic processes during HCC progression. Mechanistically, histone lactylation in HCC induces increased expression of YTHDC1, increasing the stability of m6A-modified NEAT1. The histone acetyltransferase p300 is then recruited by NEAT1 and activates SCD by increasing the level of histone acetylation at the SCD promoter, thus facilitating HCC progression via hepatocellular lipid metabolism remodeling. Taken together, these discoveries suggest a close link between the epigenetic machinery and lipid metabolic abnormalities, which promotes cancer progression.
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