Open AccessAdvanced glycation end products promote ChREBP expression and cell proliferation in liver cancer cells by increasing reactive oxygen species
Author(s) -
Hanbei Chen,
Yakui Li,
Yemin Zhu,
Lifang Wu,
Jian Meng,
Na Lin,
Dianqiang Yang,
Minle Li,
Wenjin Ding,
Xuemei Tong,
Qing Su
Publication year - 2017
Publication title -
medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.59
H-Index - 148
eISSN - 1536-5964
pISSN - 0025-7974
DOI - 10.1097/md.0000000000007456
Subject(s) - glycation , cell growth , apoptosis , carbohydrate responsive element binding protein , reactive oxygen species , western blot , cell cycle , liver cancer , cancer cell , cell , cancer research , cancer , medicine , microbiology and biotechnology , biology , transcription factor , biochemistry , receptor , gene
The aim of the study was to elucidate the mechanism by which advanced glycation end products (AGEs) promote cell proliferation in liver cancer cells. We treated liver cancer HepG2 cells with 200 mg/L AGEs or bovine serum albumin (BSA) and assayed for cell viability, cell cycle, and apoptosis. We performed real-time PCR and Western blot analysis for RNA and protein levels of carbohydrate responsive element-binding protein (ChREBP) in AGEs- or BSA-treated HepG2 cells. We analyzed the level of reactive oxygen species (ROS) in HepG2 cells treated with AGEs or BSA. We found that increased S-phase cell percentage and decreased apoptosis contributed to AGEs-induced liver cancer cell proliferation. Real-time PCR and Western blot analysis showed that AGEs stimulated RNA and protein levels of ChREBP, a transcription factor promoting glycolysis and maintaining cell proliferation in liver cancer cells. Intriguingly, the level of ROS was higher in AGEs-treated liver cancer cells. Treating liver cancer cells with antioxidant N -acetyl cystein (NAC) partly blocked AGEs-induced ChREBP expression and cell proliferation. Our results suggest that the AGEs-ROS-ChREBP pathway plays a critical role in promoting ChREBP expression and liver cancer cell proliferation.