LncRNA MEG3 Restrains Hepatic Lipogenesis via the FOXO1 Signaling Pathway in HepG2 Cells

被引：2
|
作者：
Meng, Xiangyu [1 ]
Long, Mei [2 ]
Yue, Nanxi [3 ]
Li, Quan [4 ]
Chen, Jia [4 ]
Zhao, Hongye [3 ]
Deng, Wei [4 ]
机构：
[1] Capital Med Univ, Beijing Jishuitan Hosp, Cent Lab, Beijing 100035, Peoples R China
[2] ZiBo Cent Hosp, Dept Cardiol, Zibo 255000, Shandong, Peoples R China
[3] Hebei Med Univ, Dept Biochem & Mol Biol, Key Lab Neural & Vasc Biol, Minist Educ China, Shijiazhuang 050017, Hebei, Peoples R China
[4] Capital Med Univ, Beijing Jishuitan Hosp, Dept Endocrinol, Beijing 100035, Peoples R China
来源：
CELL BIOCHEMISTRY AND BIOPHYSICS | 2024年 / 82卷 / 02期
关键词：
NAFLD; LncRNA MEG3; FOXO1; Lipid metabolism; TNF; EXPRESSION;
D O I：
10.1007/s12013-024-01278-w
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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.
引用
收藏
页码：1253 / 1259
页数：7
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