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MiR-216b suppresses cell proliferation, migration, invasion, and epithelial–mesenchymal transition by regulating FOXM1 expression in human non-small cell lung cancer
- Source :
- OncoTargets and Therapy.
- Publication Year :
- 2019
- Publisher :
- Dove Press, 2019.
-
Abstract
- Lidong Wang,1 Yansen Wang,1 Xiangyang Du,1 Yanfen Yao,2 Lei Wang,1 Yawei Jia31Department of Respiration, Shandong Provincial Third Hospital, Jinan 250031, Shandong, People’s Republic of China; 2Department of Intensive Care Unit, Shandong Provincial Third Hospital, Jinan 250031, Shandong, People’s Republic of China; 3Department of Occupational Pulmonary Disease, Shandong Academy of Occupational Health and Occupational Medicine, Jinan 250002, Shandong, People’s Republic of ChinaBackground/aims: MiR-216b and forkhead box M1 (FOXM1) were demonstrated to exert their biological effects on the development and progression of tumors. This study aimed to investigate the expression and role of miR-216b and FOXM1 in tissues and cell lines of non-small cell lung cancer (NSCLC).Methods: The expressions of miR-216b and FOXM1 in NSCLC tissues and cells were detected by qRT-PCR and Western blot analysis. Cell proliferation was measured by CCK-8 assay. Cell migration and invasion were confirmed by Transwell assay. Finally, the bioinformatics and dual-luciferase reporter assay were conducted to validate the relationship of miR-216b and FOXM1.Results: Compared with normal tissues and cells, the expression of miR-216b was obviously decreased in NSCLC tissues and cells. However, the expressions of FOXM1 mRNA and protein were significantly increased, and negatively correlated with the expression of miR-216b. Multivariate Cox’s regression analysis suggested that miR-216b or FOXM1 expression was an independent prognostic factor for patients with NSCLC. MiR-216b overexpression remarkably repressed cell proliferation, migration, invasion, and epithelial–mesenchymal transition (EMT) of NSCLC cells. The bioinformatics and dual-luciferase reporter assay validated that the 3ʹ-untranslated region (3ʹ-UTR) of FOXM1 mRNA was indeed a direct target of FOXM1. In vitro, overexpression of FOXM1 partially eliminated inhibitory effects of miR-216b on cell proliferation, migration, and invasion, whereas inhibition of FOXM1 contributed to inhibitory effects mediated by miR-216b.Conclusion: MiR-216b inhibits cell proliferation, migration, invasion, and EMT by targeting the expression of FOXM1 in human NSCLC. These findings suggested a potential therapeutic role of miR-216b in patients of NSCLC.Keywords: MiR-216b, FOXM1, NSCLC, suppressor&nbsp
- Subjects :
- 0301 basic medicine
Reporter gene
medicine.diagnostic_test
Cell growth
Cell migration
Biology
medicine.disease
OncoTargets and Therapy
03 medical and health sciences
030104 developmental biology
0302 clinical medicine
Oncology
Western blot
Cell culture
030220 oncology & carcinogenesis
Cancer research
medicine
FOXM1
Pharmacology (medical)
Epithelial–mesenchymal transition
Lung cancer
Subjects
Details
- Language :
- English
- ISSN :
- 11786930
- Database :
- OpenAIRE
- Journal :
- OncoTargets and Therapy
- Accession number :
- edsair.doi.dedup.....c1b16bd5f3898731f8134be504044514