miR-26a抑制胃癌AGS细胞生长的分子机制

The mechanism of miR-26a inhibiting gastric cancer cells proliferation

目的检测miR-26a在胃癌组织的表达改变,明确miR-26a调控胃癌细胞生长的分子机制。方法运用qRT-PCR检测71例胃癌及相应癌旁正常组织中miR-26a的表达改变;将miR-26a模拟物转染胃癌细胞AGS,采用Western blot检测其对MTDH蛋白表达水平的影响;然后采用MTT法检测高表达miR-26a对AGS细胞生长增殖的影响。结果 qRT-PCR检测结果显示,miR-26a在71例胃癌组织中表达下调0.44倍;Western blot结果显示,过表达miR-26a或干扰MTDH可抑制MTDH蛋白的表达。MTT检测发现,转染MTDH siRNA和miR-26a模拟物组AGS细胞从48 h起OD值分别为(0.158±0.006)、(0.201±0.006),与对照组细胞相比(0.515±0.032)、(0.479±0.028),差异均有统计学意义(P<0.05)。结论 miR-26a通过靶向调控MTDH的表达而抑制胃癌细胞的生长。

Objective To explicit the expression and role of miR-26a in gastric cancer tissues, thus to reveal molecular mechanism that miR-26a functions in gastric cancer ceils. Methods The qRT-PCR was conducted for detect the ex- pression of miR-26a in 71 cases of gastric cancers. AGS ceils were transfected with miR-26a mimics, then Western blot was performed to detect the expressions of MTDH protein. The proliferation ability of AGS cells evaluated by MTT assy. Results qRF-PCR showed that miR-26a was down-regulated 0.44 times in 71 cases of gastric cancer tissues. Western blot showed that the expressions of MTDH protein was inhibited by restored miR-26a or MTDH siRNA in AGS ceils. Overexpression of miR-26a or MTDH siRNA inhibited the proliferation of AGS ceils. Their OD values of transfected miR-26a mimics and MTDH siRNA were （0.158±0.006）,（0.201±0.006） respectively, and their OD values of transfected control were （0.515 ±0.032）, （0.479±0.028） respectively, there were statistically significance （P〈0.05）. Con- clusion miR-26a suppresses cell proliferation by targeting MTDH in gastric cancer.