Open AccessMalic enzyme 2 promotes the progression of hepatocellular carcinoma via increasing triglyceride production
Author(s) -
Zhang Shuai,
Cheng ZhiMei,
Yu JiaLI,
Lu Kai,
Xu ShengJie,
Lu Yuan,
Liu Ting,
Xia BaiJuan,
Huang Zhi,
Zhao XuYa,
He Wei,
Li JunXiang,
Cao Wei,
Huang Yu,
Wang Ling,
Zeng Zhu,
Zou Xun,
Liu Rong,
Zhang YuSui,
Wu XiaoPing,
Jiang TianPeng,
Zhou Shi
Publication year - 2021
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.4209
Subject(s) - triglyceride , malic enzyme , gene knockdown , hepatocellular carcinoma , apoptosis , gene silencing , cancer research , cell growth , carcinogenesis , biology , enzyme , cell cycle , cancer , endocrinology , medicine , cholesterol , biochemistry , gene , dehydrogenase
The incidence and mortality of hepatocellular carcinoma (HCC) are gradually increasing during the past years. Recently, some studies have reported that malic enzyme (ME) plays an important role in cancer development, while the involvement of ME2 in HCC remains still undetermined. Here, we demonstrated that ME2 played an oncogenic role in HCC. ME2 was overexpressed in HCC tissues. TCGA database showed that the ME2 transcript level was inversely associated with the survival of HCC patients. Loss‐of‐function and gain‐of‐function assays showed that ME2 promoted HCC cell growth and migration. Furthermore, the xenografted tumorigenesis of MHCC97H cells was retarded by ME2 knockdown. ME2 silencing also suppressed the cell cycle process and induced apoptosis. Mechanistically, ME2 potentiated triglyceride synthesis, inhibition of which suppressed the proliferation and migration. We propose that ME2 promotes HCC progression by increasing triglyceride production.