Malic enzyme 2 promotes the progression of hepatocellular carcinoma via increasing triglyceride production
Shuai Zhang, Zhimei Cheng, Jiali Yu, Kai Lǚ, Shengjie Xu, Yuan Lü, Ting Liu, Baijuan Xia, Zhi Huang, Xuya Zhao, Wei He, Junxiang Li, Wei Cao, Yu Huang, Ling Wang, Zhu Zeng, Xun Zou, Rong Liu, Yusui Zhang, Xiaoping Wu, Tianpeng Jiang, Shi Zhou
Abstract
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.