【摘要】 目的 :探讨lncRNA SNHG15对子宫内膜癌细胞(EC)增殖及去集蛋白-金属蛋白酶17(ADAM17)表达的影响。方法 :选择2018年12月—2019年12月南阳市中心医院手术子宫内膜癌组织及癌旁组织,通过PCR检测lncRNA SNHG15水平;Ishikawa细胞分为EC组(无转染),NC组(转染si-NC),实验组(转染lncRNA SNHG15-siRNA),通过CCK-8、Transwell小室、流式细胞仪检测Ishikawa细胞增殖、侵袭及凋亡,免疫印迹检测ADAM17蛋白相关表达量。结果 :LncRNA SNHG15在内膜癌组织中的表达水平显著高于癌旁组织;EC组及NC组Ishikawa细胞活力OD值差异无统计学意义。24、48、72 h时,实验组与EC组相比,Ishikawa细胞活力OD值明显降低,表明敲低lncRNA SNHG15能够抑制EC活力;EC组、NC组细胞侵袭数显著高于实验组;EC组、NC组细胞凋亡率显著低于实验组;EC组、NC组ADAMl7蛋白表达水平显著高于实验组。结论 :敲低lncRNA SNHG15能够抑制EC增殖及侵袭,凋亡加剧,其机制可能与降低ADAM17水平相关。更多还原

【Abstract】 Objective : To explore the effect of lncRNA SNHG15 on the proliferation of endometrial cancer(EC) cells and the expression of ADAM17. Methods : EC tissues and adjacent cancer tissues were selected in our hospital from December 2018 to December 2019, and the lncRNA SNHG15 level was detected by PCR. The EC cells cultured in vitro were divided into EC group(no transfected Ishikawa cells), NC group(Ishikawa cells transfected with si-NC), experimental group(Ishikawa cells transfected with lncRNA SNHG15-siRNA). CCK-8, transwell chamber and flow cytometry were used to detect Ishikawa cells proliferation, invasion and apoptosis, and immunoblotting was used to detect the expression of ADAM17 protein. Results : The levels of lncRNA SNHG15 in EC tissues were significantly higher than those in adjacent tissues. There was no difference in the OD value of Ishikawa cell viability between EC group and NC group. Compared with EC group, the OD value of Ishikawa cell viability was significantly reduced in the experimental group at 24, 48, 72 h, indicating that knocking down lncRNA SNHG15 could inhibit Ishikawa cell viability. The number of invased cells in the EC group and the NC group was significantly more than that in experimental group. Apoptosis rate in the EC group, NC group was significantly lower than that in the experimental group. The expression of ADAM17 protein in the EC group and NC group was significantly higher than that in the experimental group. Conclusion : Knocking down lncRNA SNHG15 can inhibit the proliferation and invasion of EC, and the apoptosis is intensified. The mechanism may be related to the reduction of ADAM17 levels.更多还原