Convallatoxin Inhibits Cell Proliferation and Induces Cell Apoptosis by Attenuating the Akt-E2F1 Signaling Pathway in K562 Cells

Abstract

Objective: To determine the effect of convallatoxin on K562 cell proliferation and apoptosis. Methods: CCK-8 assay was used to detect cell proliferation; PI staining, JC-1 staining, and Annexin V-FITC/PI double staining were used to analyze the cell cycle, cell mitochondrial membrane potential, and cell apoptosis; and Western blotting was used to detect cleaved caspase-9, cleaved caspase-3, Bcl-2, Bax, and E2F1 expression and Akt phosphorylation. Subsequently, AutoDock software was used to determine the interaction between convallatoxin and Akt1. Results: Upon treatment with convallatoxin, the proliferation of K562 cells was inhibited, the cells were arrested at the S and G2/M phases, and cell apoptosis was significantly induced. In addition, Akt phosphorylation and E2F1 expression were significantly decreased, whereas E2F1 overexpression rescued convallatoxin-induced cell proliferation and apoptosis. In addition, a molecular docking assay indicated that convallatoxin could bind to Akt1. Conclusion: Convallatoxin inhibited cell proliferation and induced mitochondrial-related apoptosis in K562 cells by reducing the Akt-E2F1 signaling pathway, indicating that it is a potential agent for treating leukemia.