目的:研究microRNA 203(miR-203)对胃癌EIF5A2表达的影响,为进一步阐明miR-203与胃癌的关系提供理论基础。方法:分别应用免疫荧光化学和免疫组织化学检测胃癌细胞和组织中EIF5A2的表达;脂质体miR-203转染干预胃癌细胞后,Real time PCR和...目的:研究microRNA 203(miR-203)对胃癌EIF5A2表达的影响,为进一步阐明miR-203与胃癌的关系提供理论基础。方法:分别应用免疫荧光化学和免疫组织化学检测胃癌细胞和组织中EIF5A2的表达;脂质体miR-203转染干预胃癌细胞后,Real time PCR和Western blot检测细胞中EIF5A2 mRNA和蛋白的表达情况。结果:胃癌细胞株SGC7901胞浆中大量表达EIF5A2蛋白,而细胞核中表达较少;胃癌组织中EIF5A2的表达量明显升高;EIF5A2的表达在脂质体miR-203转染干预胃癌细胞后明显受到抑制。结论:胃癌细胞和组织中存在EIF5A2的表达,且miR-203显著抑制了EIF5A2的表达。展开更多
AIM: To elucidate the potential biological role of mi R-30 b in gastric cancer and investigate the underlying molecular mechanisms of mi R-30 b to inhibit metastasis of gastric cancer cells.METHODS: The expression of ...AIM: To elucidate the potential biological role of mi R-30 b in gastric cancer and investigate the underlying molecular mechanisms of mi R-30 b to inhibit metastasis of gastric cancer cells.METHODS: The expression of mi R-30 b was detected in gastric cancer cell lines and samples by reverse transcription-polymerase chain reaction. CCK-8 assays were conducted to explore the impact of mi R-30 b overexpression on the proliferation of gastric cancer cells. Flow cytometry was used to examine the effect of mi R-30 b on the apoptosis. Transwell test was used for the migration and invasion assays. Luciferase reporter assays and Western blot were employed to validate regulation of putative target of mi R-30 b.RESULTS: The results showed that mi R-30 b was downregulated in gastric cancer tissues and cancer cell lines and functioned as a tumor suppressor. Overexpression of mi R-30 b promoted cell apoptosis,and suppressed proliferation,migration and invasion of the gastric cancer cell lines AGS and MGC803. Bioinformatic analysis identified the 3'-untranslated region of eukaryotic translation initiation factor 5A2(EIF5A2) as a putative binding site of mi R-30 b. Luciferase reporter assays and Western blot analysis confirmed the EIF5A2 gene as a target of mi R-30 b. Moreover,expression levels of theEIF5A2 targets E-cadherin and Vimentin were altered following transfection of mi R-30 b mimics.CONCLUSION: Our findings describe a link between mi R-30 b and EIF5A2,which plays an important role in mediating epithelial-mesenchymal transition.展开更多
基金Supported by Beijing Municipal Natural Science Foundation of China,No.7132209The Capital Health Research and Development of Special,No.2014-3-4014
文摘AIM: To elucidate the potential biological role of mi R-30 b in gastric cancer and investigate the underlying molecular mechanisms of mi R-30 b to inhibit metastasis of gastric cancer cells.METHODS: The expression of mi R-30 b was detected in gastric cancer cell lines and samples by reverse transcription-polymerase chain reaction. CCK-8 assays were conducted to explore the impact of mi R-30 b overexpression on the proliferation of gastric cancer cells. Flow cytometry was used to examine the effect of mi R-30 b on the apoptosis. Transwell test was used for the migration and invasion assays. Luciferase reporter assays and Western blot were employed to validate regulation of putative target of mi R-30 b.RESULTS: The results showed that mi R-30 b was downregulated in gastric cancer tissues and cancer cell lines and functioned as a tumor suppressor. Overexpression of mi R-30 b promoted cell apoptosis,and suppressed proliferation,migration and invasion of the gastric cancer cell lines AGS and MGC803. Bioinformatic analysis identified the 3'-untranslated region of eukaryotic translation initiation factor 5A2(EIF5A2) as a putative binding site of mi R-30 b. Luciferase reporter assays and Western blot analysis confirmed the EIF5A2 gene as a target of mi R-30 b. Moreover,expression levels of theEIF5A2 targets E-cadherin and Vimentin were altered following transfection of mi R-30 b mimics.CONCLUSION: Our findings describe a link between mi R-30 b and EIF5A2,which plays an important role in mediating epithelial-mesenchymal transition.
