Proapoptotic Role of Potassium Ions in Liver Cells

Author:

Xia Zhenglin12,Huang Xusen3,Chen Kaiyun2,Wang Hanning2,Xiao Jinfeng2,He Ke2,Huang Rui2,Duan Xiaopeng2,Liu Hao4,Zhang Jinqian5,Xiang Guoan12

Affiliation:

1. Third Clinical Medical School of Southern Medical University, Guangzhou 510515, China

2. Department of General Surgery, The Second People’s Hospital of Guangdong Province, Southern Medical University, Guangzhou 510515, China

3. Department of Gastrointestinal Surgery, The Affiliated Hospital, Youjiang Medical University for Nationalities, Guangxi 533000, China

4. Department of Vascular Surgery, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China

5. Laboratory Medicine, The Second People’s Hospital of Guangdong Province, Southern Medical University, Guangzhou 510515, China

Abstract

Potassium channels are transmembrane proteins that selectively promote the infiltration of potassium ions. The significance of these channels for tumor biology has become obvious. However, the effects of potassium ions on the tumor or normal cells have seldom been studied. To address this problem, we studied the biological effects of L02 and HepG2 cells with ectogenous potassium ions. Cell proliferation, cell cycle, and apoptosis rate were analyzed. Our results indicated that potassium ions inhibited proliferation of L02 and HepG2 cells and promoted their apoptosis. Potassium ions induced apoptosis through regulating Bcl-2 family members and depolarized the mitochondrial membrane, especially for HepG2 cell. These biological effects were associated with channel protein HERG. By facilitating expression of channel protein HERG, potassium ions may prevent it from being shunted to procancerous pathways by inducing apoptosis. These results demonstrated that potassium ions may be a key regulator of liver cell function. Thus, our findings suggest that potassium ions could inhibit tumorigenesis through inducing apoptosis of hepatoma cells by upregulating potassium ions transport channel proteins HERG and VDAC1.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine

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