MicroRNA-671-5p inhibits cell proliferation, migration and invasion in non-small cell lung cancer by targeting MFAP3L

被引:16
作者
Ye, Junhui [1 ]
Luo, Wujun [1 ]
Luo, Lingling [1 ]
Zhai, Limin [1 ]
Huang, Pingping [1 ]
机构
[1] Peoples Hosp Sanmen, Dept Resp Med, 171 Renmin Rd, Taizhou 317100, Zhejiang, Peoples R China
关键词
microRNA-671-5p; metastasis; microfibril-associated protein 3-like; non-small cell lung cancer; proliferation; GENE SIGNATURE; EXPRESSION; BIOGENESIS; SURVIVAL;
D O I
10.3892/mmr.2021.12546
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
MicroRNA (miR)-671-5p serves as a tumor suppressor in several types of cancer, including gastric and breast cancer. However, the function of miR-671-5p in non-small cell lung cancer (NSCLC) has not been described in detail. The present study aimed to investigate the role of miR-671-5p in NSCLC. The expression levels of miR-671-5p were determined in NSCLC tissue samples and cell lines using reverse transcription-quantitative PCR. Prediction of miR-671-5p targets was performed using the TargetScan database and verified by luciferase reporter assay and western blot analysis. Functional experiments, including Cell Counting Kit-8, wound healing and Transwell assays, were performed in NSCLC cells. The results of the present study demonstrated that lower expression levels of miR-671-5p were observed in NSCLC tissues and cell lines compared with those in the corresponding controls. Low miR-671-5p levels were significantly associated with an advanced Tumor-Node-Metastasis stage and lymph node metastasis in patients with NSCLC. Microfibril-associated protein 3-like (MFAP3L) was confirmed to be a direct target of miR-671-5p. The proliferative, migratory and invasive abilities of NSCLC cells were suppressed following transfection with miR-671-5p mimics and promoted by the miR-671-5p inhibitor compared with those in the respective control groups. In addition, the effects of miR-671-5p on cell proliferation, migration and invasion, as well as the expression levels of proliferating cell nuclear antigen, E-cadherin, N-cadherin and vimentin were reversed by MFAP3L overexpression. In conclusion, targeting the miR-671-5p/MFAP3L signaling pathway may be a promising therapeutic strategy for NSCLC treatment.
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页数:8
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