Inhibitory Effects of Blockage of Intermediate Conductance Ca2＋-Activated K＋ Channels on Proliferation of Hepatocellular Carcinoma Cells

• Published in: Journal of Huazhong University of Science and Technology. Medical sciences Vol. 33; no. 1; pp. 86 - 89
• Main Author: 杨筱嵬 刘谨文 张汝超 殷茜
• Format: Journal Article
• Language: English
• Published: Heidelberg Huazhong University of Science and Technology 01.02.2013; Department of General Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China%Department of General Surgery, Yichang Central People's Hospital, the First College of Clinical Medical Science, China Three Gorges University, Yichang 443003, China
• Subjects: HepG2; Medicine; Medicine & Public Health; mRNA表达水平; Western印迹法; 人肝癌细胞株; 堵塞; 癌组织; 细胞增殖; 钙激活钾通道; channel; TRAM-34; proliferation; intermediate conductance Ca; hepatocellular carcinoma; activated K; intermediate conductance Ca2+-activated K+ channel
• ISSN: 1672-0733; 1993-1352
• DOI: 10.1007/s11596-013-1076-0

The roles of intermediate conductance Ca2＋-activated K＋ channel （IKCal） in the pathogene- sis of hepatocellular carcinoma （HCC） were investigated. Immunohistochemistry and Western blotting were used to detect the expression of IKCal protein in 50 HCC and 20 para-carcinoma tissue samples. Real-time PCR was used to detect the transcription level of IKCal mRNA in 13 HCC and 11 para-carcinoma tissue samples. The MTT assay was used to measure the function of IKCal in human HCC cell line HepG2 in vitro. TRAM-34, a specific blocker of IKCal, was used to intervene with the function of IKCal. As compared with para-carcinoma tissue, an over-expression of IKCal protein was detected in HCC tissue samples （P〈0.05）. The mRNA expression level of IKCal 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 pxnol/L） in vitro （P〈0.05）. Our results suggested that IKCal may play a role in the proliferation of human HCC, and IKCal blockers may represent a potential therapeutic strategy for HCC.