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[目的]探讨微小RNA(miR)125b-和miR-27a对肺癌细胞95D靶基因的调控作用,探索肺癌的发病机制。[方法]通过生物信息学对miR-125b和miR-27a进行靶基因预测和GO功能分析,并通过转染模拟物和抑制物的分别上调和下调细胞中miR-125b和miR-27a的表达水平,应用Western blot检测预测靶基因的蛋白表达水平。[结果]靶基因预测和GO基因功能注释结果显示:miR-125b与凋亡的调节功能有关,MAP3K11是其重要靶基因之一;miR-27a与转录和细胞分化功能有关,PLK2是其潜在靶基因之一。Western blot结果显示:与相应阴性对照组相比,miR-125b抑制物转染组MAP3K11蛋白的表达明显增高1.795倍(P<0.05),模拟物转染组MAP3K11蛋白的表达未发生明显改变(P>0.05);miR-27a抑制物和模拟物转染组PLK2蛋白的表达均未发生明显改变(P>0.05)。[结论]miR-125b可能通过对MAP3K11的调节参与MAP3K介导的凋亡,影响肺癌的发生发展。
[Objective] To investigate the regulatory effect of miR-125b- and miR-27a on 95D target gene in lung cancer cells and to explore the pathogenesis of lung cancer. [Methods] The target genes of miR-125b and miR-27a were predicted by bioinformatics and the GO function was analyzed. The expression levels of miR-125b and miR-27a were up-regulated and down-regulated by transfecting mimics and inhibitors respectively , Using Western blot detection of target protein expression levels. [Results] The results of target gene prediction and GO gene annotation showed that miR-125b is involved in the regulation of apoptosis and MAP3K11 is one of the important target genes. MiR-27a is involved in transcription and differentiation, and PLK2 is a potential target One of the genes. The results of Western blot showed that compared with the corresponding negative control group, the expression of MAP3K11 protein in miR-125b inhibitor group was significantly increased by 1.795-fold (P <0.05), while the expression of MAP3K11 protein in mock-transfected group did not change significantly > 0.05). There was no significant change in the expression of PLK2 protein in miR-27a inhibitor and mock transfected group (P> 0.05). [Conclusion] miR-125b may be involved in the MAP3K-mediated apoptosis through the regulation of MAP3K11, which may affect the occurrence and development of lung cancer.