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ATGL promotes the proliferation of hepatocellular carcinoma cells via the p‐AKT signaling pathway
Author(s) -
Liu Meiling,
Yu Xuegao,
Lin Liying,
Deng Jiankai,
Wang Kanglong,
Su Baochang,
Xia Yong,
Tang Xiaohua,
Hong Honghai
Publication year - 2019
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22391
Subject(s) - adipose triglyceride lipase , hepatocellular carcinoma , protein kinase b , downregulation and upregulation , cancer research , cell growth , chemistry , signal transduction , biology , microbiology and biotechnology , adipose tissue , biochemistry , lipolysis , gene
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.