Effect of AZD5363 on apoptosis and autophagy in hepatocellular carcinoma cells
10.3969/j.issn.1000-4718.2019.02.015
- VernacularTitle:AZD5363诱导肝癌细胞凋亡与自噬的实验研究
- Author:
Ruo-Tong LI
1
Author Information
1. 泰安市中心医院病理科
- Keywords:
Hepatocellular carcinoma;
Akt signaling pathway;
AZD5363;
Apoptosis;
Autophagy
- From:
Chinese Journal of Pathophysiology
2019;35(2):280-285
- CountryChina
- Language:Chinese
-
Abstract:
AIM:To investigate the effect of AZD5363, an inhibitor of Akt, on the viability, apoptosis and autophagy in human hepatocelluar carcinoma cells and the molecular mechanisms.METHODS:MTT assay was used to detect the cell viability.TUNEL assay was used to analysis the apoptosis.The expression of PARP and LC3-II proteins was examined by Western blot analysis.The autophagy was characterized by the expression and distribution of GFP-LC3.RE-SULTS:The results of MTT assay indicated that AZD5363 suppressed the cell viability in a dose-dependent manner (P<0.05).High doses of AZD5363 triggered apoptosis via activating the cleavage of PARP.AZD5363 treatment induced autophagy both in Hep G2 cells and Huh7 cells by increasing the level of LC3-II.Blockage of autophagy by chloroquine promoted AZD5363-induced apoptosis in the hepatocellular carcinoma cells.CONCLUSION:AZD5363 increased apoptosis and autophagy in Hep G2 cells and Huh7 cells.Blockage of autophagy magnified AZD5363-induced apoptosis in hepatocellular carcinoma cells.
