摘要
目的探究miR-34a通过组蛋白去乙酰化酶1(HDAC1)调控子宫内膜癌(EC)细胞增殖和凋亡的机制。方法网站预测和荧光素酶实验验证miR-34a靶向HDAC1。人EC细胞系HEC-1A分为对照组、mimic组、mimic+HDAC1组和HDAC1组。通过转染miR-34a类似物(mimic)或(和)HDAC1 pcDNA以上调miR-34a或(和)HDAC1的水平。检测比较4组HEC-1A细胞中miR-34a、HDAC1 mRNA的相对表达水平以及细胞活力和凋亡率情况。并分析4组HEC-1A细胞中HDAC1、Wnt1和β-catenin蛋白表达水平。结果与对照组比较,mimic组和mimic+HDAC1组miR-34a表达水平显著升高,HDAC1组HDAC1 mRNA和蛋白的表达水平也显著升高(P<0.05)。mimic组HDAC1 mRNA和蛋白表达水平低于对照组(P<0.05)。mimic+HDAC1组HDAC1 mRNA和蛋白的表达水平高于mimic组(P<0.05)。与对照组比较,mimic组的细胞活力、Wnt1和β-catenin蛋白表达水平显著降低,而凋亡率升高(P<0.05)。HDAC1组的细胞活力、Wnt1和β-catenin蛋白表达水平显著高于对照组,而凋亡率低于对照组(P<0.05)。并且mimic+HDAC1组的细胞活力、Wnt1和β-catenin蛋白表达水平显著高于mimic组,而凋亡率低于mimic组(P<0.05)。结论miR-34a可通过靶向调节HDAC1的水平调节EC细胞的增殖和凋亡,这种调节作用可能通过影响Wnt/β-catenin通路实现。
Objective To investigate the mechanism of miR-34a regulating the proliferation and apoptosis of endometrial cancer(EC)cells through histone deacetylase 1(HDAC1).Methods Website prediction and luciferase experiments verified that miR-34a targets HDAC1.Human EC cell line HEC-1A was divided into control group,mimic group,mimic+HDAC1 group and HDAC1 group.The levels of miR-34a or(and)HDAC1 were up-regulated by transfection of miR-34a analogs(mimic)or(and)HDAC1 pcDNA.The relative expression levels of miR-34a and HDAC1 mRNA,and cell viability and apoptotic rates in HEC-1A cells of four groups were detected and compared.The expression levels of HDAC1,Wnt1 andβ-catenin protein in HEC-1A cells of four groups were analyzed.Results Compared with the control group,the expression level of miR-34a in mimic group and mimic+HDAC1 group was significantly increased and HDAC1 mRNA and protein expression levels were also significantly increased in the HDAC1 group(P<0.05).The expression levels of HDAC1 mRNA and protein in mimic group were lower than those in control group(P<0.05).The expression levels of HDAC1 mRNA and protein in mimic+HDAC1 group were higher than those in mimic group(P<0.05).Compared with the control group,the cell viability,Wnt1 andβ-catenin protein expression levels in the mimic group were significantly reduced,while the apoptosis rate was increased(P<0.05).The cell viability,Wnt1 andβ-catenin protein expression levels of the HDAC1 group were significantly higher than those of the control group,while the apoptosis rate was lower than that of the control group(P<0.05).The cell viability,Wnt1 andβ-catenin protein expression levels of mimic+HDAC1 group were significantly higher than those of mimic group,while the apoptosis rate was lower than that of mimic group(P<0.05).Conclusion miR-34a regulates the proliferation and apoptosis of EC cells by targeting the regulation of HDAC1,which may be achieved through the Wnt/β-catenin pathway.
作者
何武奇
罗婷娟
王沂峰
HE Wu-qi;LUO Ting-juan;WANG Yi-feng(Department of Gynecology,Zhujiang Hospital of Southern Medical University the Second Clinical Medical College,Guangzhou 510515,China;Department of Emergency,Maternal and Child Health Hospital of Guilin,Guilin,Guangxi Zhuang Autonomous Region 541000,China)
出处
《解放军医药杂志》
CAS
2020年第3期64-68,共5页
Medical & Pharmaceutical Journal of Chinese People’s Liberation Army
