Inhibitory effects of blockage of intermediate conductance Ca(2+)-activated K (+) channels on proliferation of hepatocellular carcinoma cells.
10.1007/s11596-013-1076-0
- Author:
Xiao-wei YANG
1
;
Jin-wen LIU
;
Ru-chao ZHANG
;
Qian YIN
;
Wen-zhuang SHEN
;
Ji-lin YI
Author Information
1. Department of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. xwyang@smail.hust.edu.cn
- Publication Type:Journal Article
- MeSH:
Calcium Channel Blockers;
pharmacology;
Carcinoma, Hepatocellular;
pathology;
physiopathology;
Cell Proliferation;
drug effects;
Hep G2 Cells;
Humans;
Intermediate-Conductance Calcium-Activated Potassium Channels;
antagonists & inhibitors;
metabolism;
Ion Channel Gating;
drug effects;
Liver Neoplasms;
pathology;
physiopathology;
Potassium;
metabolism;
Pyrazoles;
pharmacology;
Tumor Cells, Cultured
- From:
Journal of Huazhong University of Science and Technology (Medical Sciences)
2013;33(1):86-89
- CountryChina
- Language:English
-
Abstract:
The roles of intermediate conductance Ca(2+)-activated K(+) channel (IKCa1) in the pathogenesis of hepatocellular carcinoma (HCC) were investigated. Immunohistochemistry and Western blotting were used to detect the expression of IKCa1 protein in 50 HCC and 20 para-carcinoma tissue samples. Real-time PCR was used to detect the transcription level of IKCa1 mRNA in 13 HCC and 11 para-carcinoma tissue samples. The MTT assay was used to measure the function of IKCa1 in human HCC cell line HepG2 in vitro. TRAM-34, a specific blocker of IKCa1, was used to intervene with the function of IKCa1. As compared with para-carcinoma tissue, an over-expression of IKCa1 protein was detected in HCC tissue samples (P<0.05). The mRNA expression level of IKCa1 in HCC tissues was 2.17 times higher than that in para-carcinoma tissues. The proliferation of HepG2 cells was suppressed by TRAM-34 (0.5, 1.0, 2.0 and 4.0 μmol/L) in vitro (P<0.05). Our results suggested that IKCa1 may play a role in the proliferation of human HCC, and IKCa1 blockers may represent a potential therapeutic strategy for HCC.
