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目的探讨miR-96-5p上调对A549增殖的影响。方法 miR-96-5p干扰和高表达载体、shR-NA-mTOR分别转染二甲双胍干预和未干预的A549后,观察细胞增殖和p21、cyclin D1、p-4E-BP、p-S6K的表达,萤光素酶试验鉴定miR-96-5p的靶点mTOR。结果上调miR-96-5p可单独通过mTOR/p-4E-BP/p-S6K通路或协同二甲双胍抑制A549增殖。上调miR-96-5p可增加p21、降低cyclin D1表达,这可能与miR-96诱导的G1期阻滞有关。mTOR野生型3′UTR组萤光比值显著低于空白对照组和突变型组。结论miR-96-5p通过靶向mTOR抑制A549增殖。
Objective To investigate the effect of miR-96-5p upregulation on the proliferation of A549. METHODS: The miR-96-5p interference and high expression vector and shR-NA-mTOR were transfected with metformin alone and non-intervented A549 cells. Cell proliferation and expression of p21, cyclin D1, p-4E-BP and p-S6K were observed. The luciferase assay identified the target mTOR for miR-96-5p. Results Up-regulated miR-96-5p alone inhibited A549 proliferation through the mTOR/p-4E-BP/p-S6K pathway or in combination with metformin alone. Up-regulation of miR-96-5p increased p21 and decreased cyclin D1 expression, which may be related to miR-96-induced G1 arrest. The fluorescence ratio of the mTOR wild-type 3’ UTR group was significantly lower than that of the blank control group and the mutant group. Conclusion miR-96-5p inhibits A549 proliferation by targeting mTOR.