Effect Of The Acetoacetate Extract Of Vitex Negundo Seed On The Proliferation Of CNE-1Cell Lines In Nasopharygeal Carcinoma

Objective: To research the proliferation inhibition of the Acetoacetate Extractof Vitex Negundo Seed (Evn-50) on nasopharyngeal carcinoma CNE-1cell lines. Toexplore the value of its clinical treatment in nasopharyngeal carcinoma.Methods: Human nasopharyngeal carcinoma CNE-1cell lines were culturedin vitro. The cell proliferation inhibition and IC50of CNE-1cells was detected by CellCounting Kit-8assay. The proliferation and cell cycle of CNE-1cells was analyzed byflow cytometry with PI staining. The expression of cell cycle-related proteins p27andCDK2in CNE-1cells was detected by RT-PCR and Western Blotting.Results:1. CCK-8assay showed that Evn-50significantly inhibited the proliferation ofCNE-1cells in a dose-and time-dependant manner and the value of IC50was2.5ug/ml.2. Flow cytometry analysis showed that the cell proliferation of CNE-1wasobviously inhibited after treatment with2.5ug/ml Evn-50at different time and thecells in G0/G1phase were significantly increased, while the cells in S/G2/M phasewere significantly decreased in a time-dependent manner.3. RT-PCR results showed that the expression of the G1-S phase suppressorprotein p27mRNA in CNE-1cells were increased, while the expression of the G1-Sphase promoting protein CDK2mRNA were decreased after treatment with2.5ug/mlEvn-50at different time, in a time-dependent manner.4. Western blotting results showed that the expression of the G1-S phasesuppressor protein p27in CNE-1cells were increased, while the expression of the G1-S phase promoting protein CDK2were decreased after treatment with2.5ug/mlEvn-50at different time, in a time-dependent manner.Conclusion:1. Evn-50significantly inhibited the proliferation of CNE-1cells. The inhibitoryeffect was time-and dose-dependent.2. Evn-50probably inhibited the proliferation of CNE-1cells by blocking theprogress of cell cycle (G1-S phase).3. Evn-50inhibited the proliferation of CNE-1cells by up-regulating theexpression of the G1-S phase suppressor protein p27and down-regulating theexpression of the G1-S phase promoting protein CDK2.