The Central Laboratory, Beijing Jishuitan Hospital, Capital Medical University, Beijing, 100035, China.
Department of Cardiology, ZiBo Central Hospital, Zibo, Shandong, 255000, China.
Cell Biochem Biophys. 2024 Jun;82(2):1253-1259. doi: 10.1007/s12013-024-01278-w. Epub 2024 May 7.
Nonalcoholic fatty liver disease (NAFLD) become a main public health concern, and is characterized by lipid accumulation in the hepatocytes. We found that overexpression of lncRNA MEG3 significantly reduced the expression of FOXO1, ACC1, and FAS, and subsequently decreased the lipid accumulation in HepG2 cells. Moreover, inhibition of lncRNA MEG3 could increase the lipid accumulation and the mRNA and protein levels of FOXO1, ACC1, and FAS. Further study showed that lncRNA MEG3 regulates the lipogenesis process by inhibiting the entry of FOXO1 into the nucleus translocation. Our study demonstrated that lncRNA MEG3 regulates de novo lipogenesis by decreasing the expression and nucleus translocation of FOXO1 in HepG2 cells, suggesting that lncRNA MEG3 could be a promising therapeutic target in lipid metabolic disorders.
非酒精性脂肪性肝病(NAFLD)成为主要的公共卫生关注点,其特征为肝细胞内脂质蓄积。我们发现,lncRNA MEG3 的过表达显著降低了 FOXO1、ACC1 和 FAS 的表达,进而减少了 HepG2 细胞中的脂质蓄积。此外,lncRNA MEG3 的抑制可增加脂质蓄积以及 FOXO1、ACC1 和 FAS 的 mRNA 和蛋白水平。进一步的研究表明,lncRNA MEG3 通过抑制 FOXO1 进入核转位来调节脂肪生成过程。本研究表明,lncRNA MEG3 通过降低 HepG2 细胞中 FOXO1 的表达和核转位来调节从头脂肪生成,提示 lncRNA MEG3 可能成为脂质代谢紊乱的有前途的治疗靶点。