期刊
ONCOLOGY LETTERS
卷 10, 期 4, 页码 1979-1984出版社
SPANDIDOS PUBL LTD
DOI: 10.3892/ol.2015.3554
关键词
rosiglitazone; peroxisome proliferator-activated receptor gamma; phosphoinositide 3-kinase/protein kinase B; apoptosis; proliferation
类别
资金
- National Natural Foundation of China [81100264]
The inhibition of apoptosis in cancer cells is the major pathological feature of hepatic carcinoma. Rosiglitazone (RGZ), a ligand for peroxisome proliferator-activated receptor gamma (PPAR-gamma), has been shown to induce apoptosis in hepatic carcinoma cells. However, the mechanism underlying this effect remains to be elucidated. The present study aimed to investigate the effect of RGZ on cell viability and apoptosis, and its mechanisms in cultured HepG2 cells using MTT assay, flow cytometry and western blotting. The results revealed that treatment with RGZ may attenuate HepG2 cell viability and induce the apoptosis of the cells. The mechanism of RGZ-induced apoptosis involves an increase in the level of activated PPAR-gamma (p-PPAR-gamma) and a decrease in p85 and Akt expression. In addition, the PPAR-gamma antagonist GW9662 suppressed the effect of RGZ in the HepG2 cells. Taken together, the results suggest that RGZ induces the apoptosis of HepG2 cells through the activation of PPAR-gamma, suppressing the activation of the PI3K/Akt signaling pathway. Such mechanisms may contribute to the favorable effects of treatment using RGZ in HepG2 cells.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据