[Lithium chloride arrests HK-2 cell cycle in G2 phase through AKT/GSK-3β signal pathway]

[氯化锂通过AKT/GSK-3β信号通路将HK-2细胞周期阻滞在G2期]

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Abstract

OBJECTIVE: To investigate the effect of lithium chloride (LiCl) on cell cycle of HK-2 cells and explore the possible pathways involved. METHODS: HK-2 cells were treated with LiCl at different concentrations (5, 12.5, 20, and 25 mmol/L) for 12, 24, 48, or 72 h, and the changes in cell cycle and viability were detected using flow cytometry and CCK-8 assay, respectively. Western blotting was used to analyze the changes in the expressions of cyclin B1 and CDK1 (the two G2 phase-related proteins) and those of AKT/GSK-3β signaling pathway-related proteins in the treated cells. RESULTS: LiCl treatment time- and concentration-dependently increased HK-2 cell percentage in G2 phase and decreased the cell vitality. The expressions of cyclin B1, CDK1, p-GSK-3β, and β-catenin increased and the expression of p-AKT decreased significantly in the cells as LiCl treatment time and concentration increased. CONCLUSION: LiCl may cause HK-2 cell cycle arrest in G2 phase through activation of the AKT/GSK-3β signaling pathway.

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