The role of mir-221/222 in inhibiting endoplasmic reticulum stress-induced human hepatocarcinoma cell apoptosis.
- VernacularTitle:miR-221/222在肝癌细胞抵抗内质网应激凋亡中的作用
- Author:
You-Ping LIU
1
;
Chun-Yan ZHANG
;
Chuan-Ning CHEN
;
Dong-Mei YAN
;
Shao-Kun CHEN
;
Juan LI
;
Hong LI
;
Rong-Yang DAI
Author Information
- Publication Type:Journal Article
- MeSH: Apoptosis; Carcinoma, Hepatocellular; metabolism; pathology; Cell Cycle; Cell Line, Tumor; Cyclin-Dependent Kinase Inhibitor p27; metabolism; Endoplasmic Reticulum; metabolism; Humans; Liver Neoplasms; metabolism; pathology; MicroRNAs; metabolism
- From: Chinese Journal of Hepatology 2011;19(3):191-195
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of miR-221/222 in inhibiting endoplasmic reticulum stress-induced human hepatocarcinoma cells apoptosis.
METHODmiR-221/222 mimics and inhibitors were used to mimic or block the function of endogenous miR-221/222 respectively. Western blot and flow cytometry were used to test the effects of miR-221/222 on cell cycle and apoptosis under endoplasmic reticulum stress in human hepatocellular carcinoma cells.
RESULTSEndoplasmic reticulum stress resulted in miR-221/222 down-regulation in human hepatocellular carcinoma cells. miR-221/222 mimics and inhibitors inhibited and promoted respectively endoplasmic reticulum stress-mediated p27Kip1 induction. Moreover, p27Kip1 suppression not only resulted in reduction in the fraction of G1 phase cells, but also promoted the endoplasmic reticulum stress-mediated apoptosis in human hepatocellular carcinoma cells.
CONCLUSIONmiR-221/222 were downregulated by endoplasmic reticulum stress in human hepatocellular carcinoma cells, which subsequently protected human hepatocellular carcinoma cells against endoplasmic reticulum stress-induced apoptosis through p27Kip1 regulation.
