miR-96-5p上调抑制肺腺癌细胞A549的增殖

摘要

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 explore the effects of hsa-miR-96 to A549. Method A549 were transfected with miR-96 inhibitor/mimics and shRNA-mTOR. The proliferation were detected by MTT,the expression of p21, cyclin D1,p-4E-BP,S6K were detected via RT-PCR and WB. The luciferase assay were used to anaylse the target of miR-96. Result With or without metformin treated,up-regulated the expression of miR-96 could inhibit A549 proliferation,increase p21 expression and decrease cyclin D1 expression instead. The results may related with G1 arrest which induced by miR-96 up-regulation. The ratio of firefly fluorescence value/Renilla fluorescence value was lower than that in wild type NC or mutant group. Conclusion miR-96 target with mTOR to inhibit the growth of A549.