Zhao MengYang, Tang ZiBo, Wang YiJun, Ding JiaoJiao, Guo Ying, Zhang Ning, Gao TianHui
Department of Oncology, Henan Provincial People's Hospital, People's Hospital of Zhengzhou University, Zhengzhou, Henan, 450003, China.
Shenzhen People's Hospital, The Second Clinical Medical College of Jinan University, Shenzhen 518020, China.
J Cancer. 2021 Sep 13;12(22):6600-6609. doi: 10.7150/jca.60724. eCollection 2021.
Lung cancer is a serious threat to human health due to its high morbidity and mortality. microRNAs (miRNAs) are involved in the tumorigenesis and progression of lung cancer. In this study, we elucidated the role of miRNA-4507 (miR-4507) in the pathogenesis of non-small-cell lung cancer (NSCLC). miR-4507 is found to be upregulated in NSCLC cells (A549, H460). MTT, 5-ethynyl-2'-deoxyuridine (EdU), wound healing, and transwell assays were performed to evaluate NSCLC cell proliferation and migration. The results demonstrated that miR-4507 inhibition significantly decrease the proliferation and migration of NSCLC cells. Subsequently, a luciferase activity assay was conducted to verify the regulation of the predicted gene target of miR-4507, namely, . Mechanism experiments show that miR-4507 activates the PI3K/AKT signal. Further, we co-transfected miR-4507 mimics and plasmids and found that overexpression could recover the effects of miR-4507 mimics on proliferation, migration, and the PI3K/AKT signal activation. These results suggested that miR-4507 targets to facilitate the proliferation and migration of lung cancer cells through PI3K/AKT signal and that miR-4507 could serve as a potential target for NSCLC treatment.
肺癌因其高发病率和高死亡率对人类健康构成严重威胁。微小RNA（miRNA）参与肺癌的发生和发展。在本研究中，我们阐明了miRNA - 4507（miR - 4507）在非小细胞肺癌（NSCLC）发病机制中的作用。发现miR - 4507在NSCLC细胞（A549、H460）中上调。进行MTT、5 - 乙炔基 - 2'-脱氧尿苷（EdU）、伤口愈合和Transwell实验以评估NSCLC细胞的增殖和迁移。结果表明，抑制miR - 4507可显著降低NSCLC细胞的增殖和迁移。随后，进行荧光素酶活性测定以验证miR - 4507预测基因靶点即 的调控。机制实验表明，miR - 4507激活PI3K/AKT信号。此外，我们共转染miR - 4507模拟物和 质粒，发现 过表达可恢复miR - 4507模拟物对增殖、迁移和PI3K/AKT信号激活的影响。这些结果表明，miR - 4507靶向 通过PI3K/AKT信号促进肺癌细胞的增殖和迁移，并且miR - 4507可作为NSCLC治疗的潜在靶点。
