胃癌中miR-216a表达的变化及其对胃癌细胞侵袭的靶向调控作用

Changes of miR-216a expression in gastric cancer and its targeting regulation effect on invasion of gastric cancer cells

目的:研究胃癌中微小RNA-216a(miR-216a)表达的变化及其对胃癌细胞侵袭的靶向调控作用。方法:收集胃癌组织及癌旁组织,检测miR-216a的表达量;培养SGC7901细胞株并分为转染阴性对照(NC)模拟物的NC组、转染miR-216a模拟物的miR-216a组,检测穿膜细胞数、侵袭基因基质金属蛋白酶2(MMP2)、MMP9、N-钙黏蛋白(N-cadherin)及信号通路分子Janus相关激酶2(JAK2)、信号传导及转录激活因子3(STAT3)的表达量。结果:胃癌组织中miR-216a的表达量明显低于癌旁组织(P<0.05),且TNM分期、低未分化Ⅲ期、有淋巴结转移的胃癌中miR-216a的表达量明显低于TNM分期Ⅰ-Ⅱ期、中高分化、无淋巴结转移的胃癌(P<0.05);miR-216a组SGC7901细胞的穿膜数目明显少于NC组,细胞中MMP2、MMP9、N-cadherin、p-JAK2、p-STAT3的蛋白表达量及MMP2、MMP9、N-cadherin、JAK2、STAT3的mRNA表达量均明显低于NC组(P<0.05)。结论:胃癌中miR-216a的低表达能够靶向促进胃癌细胞的侵袭,且与JAK2/STAT3信号通路有关。

Objective:To study the expression of miR-216a in gastric cancer and its targeting regulation effect on invasion of gastric cancer cells.Methods: Gastric cancer tissues and adjacent tissues were collected to detect the expression of miR-216a..SGC7901 cell lines were cultured and divided into NC group transfected with negative control(NC) mimic and miR-216a group transfected with miR-216a mimic.The number of penetrating cells,the expression of invasion gene matrix metalloproteinase(MMP) 2,MMP9,N-cadherin and signaling pathway molecule janus-related kinase 2(JAK2) signal transduction and activator of transcription 3(STAT3) were detected.Results:The expression of miR-216a in gastric cancer tissues was significantly lower than that in adjacent tissues(P<0.05) and the expression of miR-216a in TNM stage Ⅲ,low undifferentiated and lymph node metastasis gastric cancer were significantly lower than those in TNM stage Ⅰ-Ⅱ,moderately well-differentiated and non-lymph node metastasis gastric cancer(P<0.05).The penetrating number of SGC7901 cells in miR-216a group was significantly less than that in NC group,and the protein expression of MMP2,MMP9,N-cadherin,p-JAK2,p-STAT3 and mRNA expression of MMP2,MMP9,N-cadherin,JAK2,STAT3 in cells was significantly lower than those in NC group(P<0.05).Conclusion:The low expression of miR-216a in gastric cancer can targetthe invasion of gastric cancer cells and this effect is related to JAK2/STAT3 signaling pathway.