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首页> 美国卫生研究院文献>Experimental and Therapeutic Medicine >MicroRNA-21 promotes the proliferation migration and invasion of non-small cell lung cancer A549 cells by regulating autophagy activity via AMPK/ULK1 signaling pathway
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MicroRNA-21 promotes the proliferation migration and invasion of non-small cell lung cancer A549 cells by regulating autophagy activity via AMPK/ULK1 signaling pathway

机译：MicroRNA-21通过AMPK / ULK1信号通路调节自噬活性促进非小细胞肺癌A549细胞的增殖迁移和侵袭

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The present study investigated the expression of microRNA (miR)-21 in non-small cell lung cancer (NSCLC) tissues, its biological functions and mechanism of autophagy regulation. A total of 46 patients with NSCLC were enrolled in the present study. To measure the expression of miR-21, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was employed. NSCLC A549 cells were transfected with miR-negative control (NC), miR-21 mimics or inhibitor. The CCK-8 assay was used to investigate the proliferation of A549 cells. To study migration and invasion abilities of A549 cells, The Transwell assay was performed. In addition, to determine the expression levels of ULK1, LC3B, AMPKα, p-AMPKα and p62 proteins, western blotting was conducted and laser confocal microscopy was performed to observe the formation of autophagosomes in A549 cells. To explore whether miR-21 regulates the biological functions of A549 cells via autophagy, an autophagy inhibitor, 3-MA, or agonist, rapamycin, were used in a rescue assay. Results indicated that miR-21 expression in NSCLC tissues was enhanced, and closely correlated with the occurrence and development of NSCLC. In vitro experiments showed that miR-21 mimics promoted the proliferation, migration and invasion of A549 cells, while miR-21 inhibitor inhibited these biological functions. Western blotting indicated that miR-21 upregulated autophagy marker LC3BII protein, but downregulated p62 protein. Laser confocal microscopy showed that miR-21 activated autophagy of A549. Rescue experiments indicated that autophagy reversed the effect of miR-21 on the proliferation, migration and invasion of A549 cells. Western blotting data suggested that autophagy-related AMPK/ULK1 signaling pathway was activated by miR-21, and interference or overexpression of ULK1 reversed the biological functions of miR-21. The present study demonstrated that miR-21 expression in NSCLC tissues was upregulated and positively correlated with lymphatic metastasis and clinical staging. In addition, miR-21 regulated autophagy activity of NSCLC A549 cells via AMPK/ULK1 signaling pathway, and promoted the proliferation, migration and invasion of NSCLC A549 cells.
机译：本研究调查了microRNA（miR）-21在非小细胞肺癌（NSCLC）组织中的表达，其生物学功能和自噬调节机制。本研究共纳入46例NSCLC患者。为了测量miR-21的表达，采用了逆转录定量聚合酶链反应（RT-qPCR）。用miR阴性对照（NC），miR-21模拟物或抑制剂转染NSCLC A549细胞。使用CCK-8测定来研究A549细胞的增殖。为了研究A549细胞的迁移和侵袭能力，进行了Transwell测定。另外，为了确定ULK1，LC3B，AMPKα，p-AMPKα和p62蛋白的表达水平，进行了蛋白质印迹，并进行了激光共聚焦显微镜观察A549细胞中自噬体的形成。为了研究miR-21是否通过自噬调节A549细胞的生物学功能，在救援分析中使用了自噬抑制剂3-MA或激动剂雷帕霉素。结果表明，miR-21在NSCLC组织中的表达增强，并且与NSCLC的发生和发展密切相关。体外实验表明，miR-21模拟物可促进A549细胞的增殖，迁移和侵袭，而miR-21抑制剂可抑制这些生物学功能。 Western印迹表明，miR-21上调了自噬标记物LC3BII蛋白，但下调了p62蛋白。激光共聚焦显微镜显示，miR-21激活了A549的自噬。救援实验表明自噬逆转了miR-21对A549细胞增殖，迁移和侵袭的作用。 Western印迹数据表明，自噬相关的AMPK / ULK1信号通路被miR-21激活，而ULK1的干扰或过表达逆转了miR-21的生物学功能。本研究表明，miR-21在非小细胞肺癌组织中的表达上调，与淋巴结转移和临床分期呈正相关。此外，miR-21通过AMPK / ULK1信号通路调节NSCLC A549细胞的自噬活性，并促进NSCLC A549细胞的增殖，迁移和侵袭。

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