本文采用的英格恩产品: Entranster-H

Upregulated microRNA‑671‑3p promotes tumor progression by suppressing forkhead box P2 expression in non‑small‑cell lung cancer

Zhi-Ying Li  ¹ , Zi-Zhou Zhang  ² , Hui Bi  ¹ , Qiu-Di Zhang  ¹ , Su-Juan Zhang  ¹ , Lin Zhou  ¹ , Xiao-Qin Zhu  ¹ , Jun Zhou  ¹ Affiliations

• PMID: 31432170
• PMCID: PMC6755202
• DOI: 10.3892/mmr.2019.10563

Free PMC article

Abstract

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.