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 cells. Methods The qRT-PCR was conducted for detect the ex-pression of miR-26a in 71 cases of gastric cancers. AGS cells 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 cells. Overexpression of miR-26a or MTDH siRNA inhibited the proliferation of AGS cells. 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.%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。
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