Inhibition of cell proliferation and arrest of cell cycle progression by blocking chloride channels in human laryngeal cancer cell line Hep-2

被引:0
|
作者
Yu, W. F. [1 ]
Zhao, Y. L. [1 ]
Wang, K. [2 ]
Dong, M. M. [1 ]
机构
[1] Zhengzhou Univ, Affiliated Hosp 1, Dept Otolaryngol, Zhengzhou 450052, Henan, Peoples R China
[2] Univ Wisconsin, Perinatal Res Labs, Dept Obstet & Gynecol, Madison, WI 53715 USA
关键词
laryngeal carcinoma; chloride channel; proliferation; cell cycle; ERK1/2; AKT1; REGULATORY VOLUME DECREASE; CYSTIC-FIBROSIS; GROWTH-FACTOR; CL-CURRENTS; AKT-KINASE; ACTIVATION; HETERODIMERIZATION; HOMODIMERIZATION; HIPPOCAMPUS; SPECIFICITY;
D O I
暂无
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Chloride channel (ClC) is involved in normal physiological processes and pathology of various diseases. Although it is recognized that blockade of ClC inhibits the cell proliferation, it is not well understood the potential function of ClC in laryngeal cancer. In this study, we investigated the effect of the ClC inhibitor on cell proliferation, cell cycle progression in human laryngeal cancer cell line Hep-2, as well as the effect on the phosphorylation levels of ERK1/2 and AKT1. In this study crystal violet method was used to study the effect of the ClC inhibitor, 5-nitro-2-(3-phenylpropylamino) benzoic acid, NPPB, on Hep-2 cell proliferation. The impaction of the inhibitor on the cell cycle distribution was investigated by the flow cytometry (FCM). Western blot was performed to measure the phosphorylation levels of ERK1/2 and AKT1. Our data indicated ClC played an important role in Hep-2 cell proliferation and cell cycle. NPPB inhibited Hep-2 cell proliferation when compared with the controls. Blockade of ClC arrested cell cycle progression and suppressed the phosphorylation of ERK1/2 and AKT1 in Hep-2 cells by inhibition of cell proliferation by ClC inhibitor (NPPB) could be through arresting cell cycle progression, which is probably by suppressing phosphorylation of ERK1/2 and AKT1.
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页码:224 / 229
页数:6
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