Department of Respiratory Medicine, The First People's Hospital of Changzhou, Changzhou, Jiangsu 213000, P.R. China.
Department of Respiratory Medicine, The Seventh People's Hospital of Changzhou, Changzhou, Jiangsu 213011, P.R. China.
Mol Med Rep. 2019 Oct;20(4):3149-3159. doi: 10.3892/mmr.2019.10563. Epub 2019 Aug 6.
In the present study, the expression of microRNA (miR)‑671‑3p in non‑small‑cell lung cancer (NSCLC) was detected via reverse transcription‑quantitative polymerase chain reaction analysis, and its role in cell proliferation, apoptosis, migration and invasion was investigated via Cell Counting Kit‑8, colony formation, flow cytometry, Transwell and scratch assays, respectively. It was observed that the expression of miR‑671‑3p was upregulated in NSCLC tissues and cell lines (A549 and H1975). Treatment with miR‑671‑3p inhibitors suppressed cell proliferation, migration and invasion, and increased apoptosis in vitro, suggesting that miR‑671‑3p functions as an oncogene in NSCLC. In addition, forkhead box P2 (FOXP2) has been reported to be a tumor suppressor that is downregulated in several types of cancer, and its low expression was confirmed in NSCLC tissues and cell lines in the current study via western blotting. The results of the luciferase reporter assay also demonstrated that miR‑671‑3p targeted directly the 3'‑untranslated region of FOXP2. Furthermore, overexpression of FOXP2 in A549 and H1975 cell lines suppressed the growth, migration and invasion, and promoted apoptosis, whereas these effects were reversed by transfection with miR‑671‑3p mimics, suggesting that miR‑671‑3p promoted tumor progression via regulating FOXP2. Taken together, the results reported in the present study implied that miR‑671‑3p may be a potential therapeutic target in NSCLC.
在本研究中,通过逆转录-定量聚合酶链反应分析检测了非小细胞肺癌(NSCLC)中 microRNA(miR)-671-3p 的表达,并通过细胞计数试剂盒-8 检测、集落形成实验、流式细胞术、Transwell 和划痕实验分别研究了其在细胞增殖、凋亡、迁移和侵袭中的作用。结果观察到 miR-671-3p 在 NSCLC 组织和细胞系(A549 和 H1975)中呈上调表达。用 miR-671-3p 抑制剂处理可抑制细胞增殖、迁移和侵袭,并增加体外凋亡,提示 miR-671-3p 在 NSCLC 中作为癌基因发挥作用。此外,叉头框蛋白 P2(FOXP2)已被报道为在多种类型的癌症中下调的肿瘤抑制因子,本研究通过 Western blot 验证了其在 NSCLC 组织和细胞系中的低表达。荧光素酶报告基因检测的结果也表明,miR-671-3p 直接靶向 FOXP2 的 3'-非翻译区。此外,在 A549 和 H1975 细胞系中过表达 FOXP2 可抑制细胞生长、迁移和侵袭,并促进凋亡,而用 miR-671-3p 模拟物转染则逆转了这些作用,提示 miR-671-3p 通过调节 FOXP2 促进肿瘤进展。综上所述,本研究结果表明,miR-671-3p 可能是 NSCLC 的潜在治疗靶点。