Matrine-induced Apoptosis Of Human Nasopharyngeal Carcinoma Cells Via In Vitro Vascular Endothelial Growth Factor-A/Extracellular Signal-regulated Kinase1/2Pathway Inactivation

Background and Objective: Now, the main treatment to nasopharyngealcarcinoma includes radiotherapy and chemotherapy, but both of them havesevere toxic side effects and making the influence of further therapy. So thedevelopment of effective but less toxic therapies is necessary. Recently, somestudies have shown that matrine can inhibit proliferation and induce apoptosisagainst a wide range of cancers, and getting widely attention. In the presentstudy, we research matrine induce apoptosis in human nasopharyngealcarcinoma via in vitro vascular endothelial growth factor-A/extracellularsignal-regulated kinase1/2pathway inactivation and explored the antitumormechanism of matrine.Methods: The proliferation inhibition treated by matrine in humannasopharyngeal carcinoma cell lines (CNE1and CNE2cells) and HUVEC weresubjected to MTT assay. Matrine-induced apoptosis in NPC cells were measuredby Hoechst33258staining and flow cytometry. The activation of caspases were examined by qRT-PCR and Western blot. In addition, the expression of VEGFAand the phosphorylation of ERK1/2were detected by Western blot.Results: We found that matrine inhibited the proliferation and inducedapoptosis of human nasopharyngeal carcinoma cell lines in vitro and induced theactivation of caspase-3,-8, and-9in a dosedependent manner. However, matrinehad no obvious effects on proliferation of HUVEC cells even at a highconcentration of4mg/ml. From the MTT assay and Hoechst33258staining, themost striking effect was observed in CNE2cells. Furthermore, matrine candecrease the expression of VEGFA and the phosphorylation of ERK1/2in adose-dependent and time-dependent manner.Condusion: Matrine could inhibit the proliferation of humannasopharyngeal carcinoma CNE1and CNE2cells. The inhibition of cellproliferation mechanism may induce cell apoptosis, expression of apoptosisrelated gene Caspase-3, Caspase-8, Caspase-9, and the expression of VEGFAand ERK1/2is down regulated, possibly by the apoptosis of VEGFA-ERK1/2MAPK-Caspase cell pathway.