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作 者:李妍[1] 孟凡东[1] 付立业[1] 蒋涛[1] 姜又红[1]
机构地区:[1]中国医科大学附属第一医院肿瘤研究所二室,辽宁沈阳110001
出 处:《现代肿瘤医学》2017年第9期1374-1377,共4页Journal of Modern Oncology
基 金:辽宁省医学高峰建设项目(编号:2010017)
摘 要:目的:探讨EZH2对胃癌MKN-28细胞生物学的影响。方法:siRNA干扰EZH2;MTT法检测沉默EZH2后细胞的增殖情况;Transwell小室观察细胞的侵袭情况;Realtime-PCR检测细胞中相关基因的表达情况。结果:siRNA有效干扰了EZH2的表达;沉默EZH2细胞组的细胞增殖明显受到抑制(P<0.05);细胞的侵袭情况,沉默EZH2明显抑制了细胞的侵袭,与其他两组比较差异显著(P<0.05);si EZH2细胞组E-cadherin mRNA、β-catenin mRNA的表达水平高于其他两组,Bcl-2 mRNA的表达水平低于其他两组(P<0.05)。结论:沉默EZH2抑制了胃癌MKN-28细胞的增殖,抑制了细胞的侵袭和抗凋亡基因的表达,可能是通过调控E-cadherin的表达水平和Wnt信号途径实现的,为寻找有效的靶点和肿瘤的靶向治疗提供一定的理论依据。Objective:To explore the biological effects on gastric MKN-28 cells by EZH2.Methods:siRNA interfered EZH2.MTT was used to detect the proliferation of cells with EZH2 silence.Transwell Chambers was used to observe invasive ability.The expression of genes in MKN-28 cells were analysed by Realtime-PCR.Results:siRNA effectively interfered the expression of EZH2.Cell proliferation were significantly suppressed in siRNA-EZH2 cell group(P〈0.05).Cell invasive experiments have shown that the number of siEZH2 group of cells was significantly lower than other groups(P〈0.05).Realtime-PCR showed that the expression of E-cadherin mRNA,β-catenin mRNA in siEZH2 group was higher than those in other groups(P〈0.05),and the expression of Bcl-2 mRNA,the siEZH2 group was lower than that in other groups(P〈0.05).Conclusion:Silence EZH2 affected gastric cancer MKN-28 cell proliferation,inhibited invasion and antiapoptotic gene expression,EZH2 may play a role by the expression of E-cadherin and the Wnt signaling pathway,and these results of the experiment provide certain theoretical basis for research the target of effective and new therapeutic targets.
关 键 词:胃癌 EZH2 E-CADHERIN Β-CATENIN BCL-2
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