Study On The Mechanism Of Apigenin Inhibits Proliferation Of Human Lung Cancer A549and H460Cells

Objective:The purpose of the study was to investigate the effect and mechanism of Apigenin inhibiting proliferation of human lung cancer A549and H460cells to provide the basis for clinical application in the future.Methods:The anti-proliferative effect of API was assessed by MTT assay. The analysis of cell cycle were evaluated by flow cytometry. The expressions of p-P53、P21、p-Wee1、Myt1、 Cyclin B、p-cdc2、P27、Cyclin A2、Cyclin E、CDK2、p-Rb and E2F1related to cell cycle were detected by Western Blot after treatment with API in vitro.Results:API suppressed the proliferation of human lung cancer A549and H460cells in a time and dose-dependent manner. Cells treated with API in6.25uM、12.5uM、25uM and50uM dose after24,48and72hours have difference with cells without treatment. The analysis of flow cytometry indicated that API blocked A549cells at G2/M phases and H460cells at S phases. Western Blot showed that after treatment with API in12.5uM、25uM and50uM dose the expression of p-P53、P21、p-Wee1and Myt1enhanced and the expression of Cyclin B and p-cdc2reduced of A549cells, the expression of p-P53、P21and P27enhanced and the expression of Cyclin A2、Cyclin E、CDK2、p-Rb and E2F1reduced of H460cells, both in a dose-dependent manner. There was difference with blank control group.Conclution:API could inhibit the proliferation of human lung cancer A549and H460cells. Cells were blockcd at G2/M and S phases respectively through evaluating expression of p-P53、P21、 p-Wee1、Myt1、Cyclin B、p-cdc2、P27、Cyclin A2、Cyclin E、CDK2、p-Rb、E2F1related with cell cycles.