Title | DDX17 protects hepatocytes against oleic acid/palmitic acid-induced lipid accumulation |
Authors | Zhang, Xiaoyi An, Tong Zhang, Xiyue Shen, Tao Li, Hongxia Dou, Lin Huang, Xiuqing Man, Yong Tang, Weiqing Li, Jian |
Affiliation | Peking Univ, Sch Clin Med 5, Beijing 100730, Peoples R China Beijing Hosp, Chinese Acad Med Sci, Beijing Inst Geriatr, Inst Geriatr Med, Beijing 100730, Peoples R China |
Keywords | RNA HELICASES MESSENGER-RNA P68 PROTEINS TRANSCRIPTION P72 |
Issue Date | 5-Jul-2022 |
Publisher | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS |
Abstract | Hepatic lipid accumulation is an initiation factor in fatty liver disease, and promoting a reduction in hepatic lipid accumulation is an important treatment strategy. DEAD box RNA helicase 17 (DDX17) is a member of the DEAD-box family and a molecular chaperone. Previous studies have demonstrated that DDX17 is a transcriptional coregulator of tumorigenesis, inflammation, and macrophage cholesterol efflux. The liver is the main site for lipid metabolism, and metabolic (dysfunction)-associated fatty liver disease (MAFLD) is one of the most common chronic liver diseases. However, the impact of DDX17 on hepatic lipid accumulation has not been verified. In this study, we found, for the first time, that oleic acid/ palmitic acid (OA/PA)-induced lipid accumulation was largely abrogated by DDX17 overexpression in both HepG2 (a human hepatocellular carcinoma line) and Hep1-6 (a murine hepatocellular carcinoma line) cells, and this effect was due to a marked reduction in cellular triglyceride (TG) content. Moreover, the overexpression of DDX17 was accompanied by a significant decrease in the expression of genes involved in de novo fatty acid synthesis (FAS, ACC, and SCD-1) in both HepG2 and Hep1-6 cells. In conclusion, DDX17 protected against OA/PA-induced lipid accumulation in hepatocytes through de novo lipogenesis inhibition.(c) 2022 Elsevier Inc. All rights reserved. |
URI | http://hdl.handle.net/20.500.11897/647483 |
ISSN | 0006-291X |
DOI | 10.1016/j.bbrc.2022.04.129 |
Indexed | SCI(E) |
Appears in Collections: | 北京医院 |