ATGL promotes the proliferation of hepatocellular carcinoma cells via the p‐AKT signaling pathway. Issue 11 (2nd September 2019)

• Record Type: Journal Article
• Authors: Liu, Meiling; Yu, Xuegao; Lin, Liying; Deng, Jiankai; Wang, Kanglong; Su, Baochang; Xia, Yong; Tang, Xiaohua; Hong, Honghai
• Is Part Of: Journal of biochemical and molecular toxicology. Volume 33:Issue 11(2019)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2019-09-02
• Subjects: ATGL -- hepatocellular carcinoma cells -- p‐AKT signaling pathway -- tumor proliferation; Biochemistry -- Periodicals; Molecular biology -- Periodicals; Toxicology -- Periodicals; 574
• DOI: 10.1002/jbt.22391
• Languages: English
• ISSNs: 1095-6670

Abstract

Abstract: Abnormal metabolism, including abnormal lipid metabolism, is a hallmark of cancer cells. Some studies have demonstrated that the lipogenic pathway might promote the development of hepatocellular carcinoma (HCC). However, the role of adipose triglyceride lipase (ATGL) in hepatocellular carcinoma cells has not been elucidated. We evaluated the function of ATGL in hepatocellular carcinoma using methyl azazolyl blue and migration assay through overexpression of ATGL in HepG2 cells. Quantitative reverse‐transcription polymerase chain reaction and Western blot analyses were used to assess the mechanisms of ATGL in hepatocellular carcinoma. In the current study, we first constructed and transiently transfected ATGL into hepatocellular carcinoma cells. Secondly, we found that ATGL promoted the proliferation of hepatoma cell lines via upregulating the phosphorylation of AKT, but did not affect the metastatic ability of HCC cells. Moreover, the p‐AKT inhibitor significantly eliminated the effect of ATGL on the proliferation of hepatoma carcinoma cells. Taken together, our results indicated that ATGL promotes hepatocellular carcinoma cells proliferation through upregulation of the AKT signaling pathway.