Objective To investigate the role of enhancer of zeste homolog 2(EZH2)and human mutL homolog 1(hMLH1)in glioma.Methods The small interfering RNA(siRNA)targeting EZH2 and hMLH1 was designed and synthesized,and transfected into U-87 cells.The control group and knockdown group were set up,and the proliferation of the two groups was analyzed through 5-Ethynyl-2'-deoxyuridine(EdU)proliferation assay.T test was used for comparison between groups.Results The results showed that the mRNA levels of EZH2(7.97±0.14,6.00±0.18,6.24±0.11,t=83.80,47.18,83.55)and hMLH1(6.15±0.08,3.93±0.17,4.25±0.12,t=103.700,29.800,45.510)were significantly higher in glioma tissues and cells than their normal counterparts(P＜0.01).Transfection of siRNA into U-87 glioma cells resulted in decreased cell proliferation capacity,with the control group being(68.2± 14.8),EZH2 knockdown group being(33.5±13.1),and hMLH1 knockdown group being(43.1± 10.0).After knocking down EZH2 and hMLH1 expression,cell apoptosis of transfected cells was en-hanced(t=3.041,2.934,P＜0.05).The ratio of p-MEK1/MEK1 and p-ERK1/ERK1 was down-regula-ted after silencing the level of p-MEK(t=5.590,6.548,P＜0.05)and p-ERK1(t=10.730,9.260,P＜0.05).The inhibitory effects were enhanced(t=6.425,7.273,P＜0.05)in U-87 cells that were co-transfected with EZH2-siRNA and hMLH1-siRNA as compared with those that were transfected individual-ly.Conclusion The findings show that the inhibition of EZH2 and hMLH1 impacts glioma growth and cell death likely via in-activating the MEK/ERK pathway.
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