LncRNA SNHG11通过抑制miR-184/CARM1信号轴促进卵巢癌生长

Influences of lncRNA SNHG11 on proliferation,apoptosis,migration and invasion of ovarian cancer cells by regulating miR-184/CARM1 signaling axis

目的探讨长链非编码RNA核仁小分子RNA宿主基因11(LncRNA SNHG11)靶向调控miR-184/CARM1信号轴对卵巢癌细胞的影响及其机制。方法实时荧光定量PCR检测卵巢癌组织与细胞中LncRNA SNHG11表达及卵巢癌细胞miR-184表达。将卵巢癌SKOV3细胞分为si-NC组、si-SNHG11组、si-SNHG11+anti-NC组、si-SNHG11+anti-miR-184组、miR-NC组、miR-184 mimics组、miR-184 mimics+pcDNA组、miR-184 mimics+CARM1组,分别检测各组细胞增殖、凋亡、迁移、侵袭及CARM1、E-cadherin、N-cadherin蛋白表达,裸鼠成瘤实验检测各组细胞在动物体内成瘤能力,双荧光素酶报告基因实验检验miR-184与LncRNA SNHG11、CARM1的靶向关系。结果LncRNA SNHG11在卵巢癌组织与细胞中表达升高,miR-184在卵巢癌细胞中表达降低(P<0.05)。与si-NC组比较,si-SNHG11组SKOV3细胞增殖、迁移与侵袭能力下降,瘤体质量与体积减小,N-cadherin表达降低,细胞凋亡率与E-cadherin蛋白表达升高(P<0.05);与si-SNHG11+anti-NC组比较,si-SNHG11+anti-miR-184组SKOV3细胞增殖、迁移与侵袭细胞能力升高,瘤体质量与体积增大,N-cadherin蛋白表达升高,细胞凋亡率与E-cadherin蛋白表达降低(P<0.05)。与miR-NC组比较,miR-184 mimics组SKOV3细胞增殖、迁移与侵袭能力下降,瘤体质量与体积减小,N-cadherin蛋白表达降低,细胞凋亡率与E-cadherin蛋白表达升高(P<0.05);与miR-184 mimics+pcDNA组比较,miR-184mimics+CARM1组SKOV3细胞增殖、迁移与侵袭能力升高,瘤体质量与体积增大,N-cadherin蛋白表达升高,细胞凋亡率与E-cadherin蛋白表达降低(P<0.05);LncRNA SNHG11靶向调控miR-184/CARM1信号轴。结论LncRNA SNHG11通过调节miR-184/CARM1信号轴,促进卵巢癌生长。

Objective To investigate the effect of long chain non coding RNA nucleolar small RNA host gene 11(lncRNA SNHG11)targeting miR-184/CARM1 signal axis on ovarian cancer cells and its mechanism.Methods Expression levels of lncRNA SNHG11 and miR-184 in ovarian cancer tissue and cells were detected by real time fluorescent quantitative PCR(qPCR),and SKOV3 cells were selected for the experiment.SKOV3 cells were divided into the si-NC group(transfected with si-NC),the si-SNHG11 group(transfected with si-SNHG11),the si-SNHG11+anti-NC group(transfected with si-SNHG11+anti-NC),the si-SNHG11+anti-miR-184 group(transfected with si-SNHG11+anti-miR-184),the miR-NC group(transfected with miR-NC),the miR-184 mimics group(transfected with miR-184 mimics),the miR-184 mimics+pcDNA group(transfected with miR-184 mimics+pcDNA)and the miR-184 mimics+CARM1 group(transfected with miR-184 mimics+pcDNA-CARM1).The cell proliferation,apoptosis,migration,invasion and the expression levels of CARM1,E-cadherin,N-cadherin protein in each group were detected respectively.The tumorigenicity of each group of cells in vivo was detected by nude mouse tumorigenesis experiment.The targeting relationship between miR-184 and lncRNA SNHG11,CARM1 was detected by double luciferase reporter gene experiment.Results The expression level of lncRNA SNHG11 was increased in ovarian cancer tissue and cells,and the expression level of miR-184 was decreased in ovarian cancer cells(P<0.05).Compared with the si-NC group,the proliferation,migration and invasion ability of SKOV3 cells were decreased in the si-SNHG11 group,and the tumor weight and volume were decreased,the expression of N-cadherin was decreased,and the apoptosis rate and the expression of E-cadherin protein were increased(P<0.05).Compared with the si-SNHG11+anti-NC group,the proliferation,migration and invasion ability of SKOV3 cells were increased in the si-SNHG11+anti-miR-184 group,the tumor weight and volume were increased,and the expression of N-cadherin protein was increased,and the apoptosis rate and E-cadherin protein expression were decreased(P<0.05).Compared with the miR-NC group,the proliferation,migration and invasion ability of SKOV3 cells were decreased in the miR-184 mimics group,the tumor weight and volume were decreased,the expression of N-cadherin protein was decreased,while the apoptosis rate and expression level of E-cadherin protein were increased(P<0.05).Compared with the miR-184 mimics+pcDNA group,the proliferation,migration and invasion ability of SKOV3 cells were increased in the miR-184mimics+CARM1 group.The tumor weight and volume were increased,and the expression of N-cadherin protein was increased,while the apoptosis rate and E-cadherin protein expression were decreased(P<0.05).LncRNA SNHG11 targetly regulated miR-184/CARM1 axis.Conclusion LncRNA SNHG11 promotes the growth of ovarian cancer by regulating miR-184/CARM1 signal axis.