microRNA-125a-5p as a Tumor Suppressor in Non-Small Cell Lung Cancer (NSCLC): Inhibition of Proliferation and Induction of Apoptosis via P13K/AKT/MMP Signaling Pathway

IF 0.9 4区 材料科学
B. Dong, Xiaowei Liu, Suo Wang, Xiujun Chen, Kun Zhang, Ying Zhang
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引用次数: 0

Abstract

To investigate the effects of micro ribonucleic acid (miR)-125a-5p on the proliferation and apoptosis of non-small cell lung cancer (NSCLC) cells and its possible mechanism. With NSCLC A549 cells as the experimental research objects, transfection reagent was employed to transfect miR-125a-5p NC group, miR-125a-5p mimic group and miR-125a-5p siRNA group into A549 cells. qRT-PCR and cloning assays were conducted to detect the level of miR125a-5p in A549 cells and the effect of miR125a-5p on the proliferation of A549 cells. The effect of miR-125a-5p on apoptosis of A549 cells was detected via FCM. Additionally, the effects of miR-125a-5p on the mRNA and protein expressions of PI3K and AKT and the expressions of MMP-2 and MMP-9 in A549 cells were determined through qRT-PCR, Western blotting and immunohistochemistry, respectively. Compared with those in miR-125a-5p NC group, the proliferation ability of A549 cells was improved, their apoptosis rate was significantly decreased, and the mRNA and protein levels of PI3K and AKT and the levels of MMP-2 and MMP-9 in A549 cells were increased in miR-125a-5p siRNA group, whereas they showed totally opposite tendencies in miR-125a-5p mimic group. miR-125a-5p overexpression can hinder A549 cell growth, boost apoptosis, and reduce MMP-2 and MMP-9 levels via the PI3K/AKT/MMP pathway.
微小RNA-125a-5p作为非小细胞肺癌(NSCLC)的肿瘤抑制剂:通过P13K/AKT/MMP信号通路抑制增殖和诱导细胞凋亡
探讨微小核糖核酸(miR)-125a-5p对非小细胞肺癌(NSCLC)细胞增殖和凋亡的影响及其可能机制。以NSCLC A549细胞为实验研究对象,采用转染试剂将miR-125a-5p NC组、miR-125a-15p模拟组和miR-125a-5p siRNA组转染到A549细胞中。进行qRT-PCR和克隆分析以检测A549细胞中miR125a-5p的水平以及miR125a-5 p对A549细胞增殖的影响。通过FCM检测miR-125a-5p对A549细胞凋亡的影响。此外,通过qRT-PCR、Western印迹和免疫组织化学分别测定了miR-125a-5p对A549细胞中PI3K和AKT的mRNA和蛋白表达以及MMP-2和MMP-9表达的影响。与miR-125a-5p-NC组相比,miR-125a-15p-siRNA组A549细胞的增殖能力提高,凋亡率显著降低,PI3K和AKT的mRNA和蛋白水平以及MMP-2和MMP-9的水平升高,而miR-125a-5p模拟组则表现出完全相反的趋势。miR-125a-5p过表达可通过PI3K/AKT/MMMP途径阻碍A549细胞生长,促进细胞凋亡,并降低MMP-2和MMP-9水平。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Science of Advanced Materials
Science of Advanced Materials NANOSCIENCE & NANOTECHNOLOGY-MATERIALS SCIENCE, MULTIDISCIPLINARY
自引率
11.10%
发文量
98
审稿时长
4.4 months
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