MiR-378 promotes the cell proliferation of non-small cell lung cancer by inhibiting FOXG1

K.-X. Ji, F. Cui, D. Qu, R.-Y. Sun, P. Sun, F.-Y. Chen, S.-L. Wang, H.-S. Sun

Department of Medical Oncology, The 2nd Affilliated Hospital of Harbin Medical University, Harbin, China. jikunxiang@126.com

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• Oncology

OBJECTIVE: To identify the functioning mode of miR-378 on non-small cell lung cancer (NSCLC) and provide therapeutic targets for NSCLC.

PATIENTS AND METHODS: Expression levels of miR-378 in human NSCLC tissue samples and NSCLC-derived cell lines were measured by using quantitative Real-time polymerase chain reaction (PCR). Cell proliferation capacity was assessed by methyl thiazolyl tetrazolium (MTT) assay and colony formation assay. Cell apoptosis and cell cycle distribution were identified by flow cytometry. Downstream target gene was confirmed by using luciferase and Western blotting assays.

RESULTS: MiR-378 was significantly elevated in NSCLC tissues when compared with para-carcinoma tissues (n=42). Decreased-miR-378 could attenuate cell proliferation capacity, as well as promoted cell apoptosis and induced cell cycle arrest at G0/G1 phase. FOXG1 was chosen as the target gene of miR-378 by bioinformatics analysis and luciferase reporter assay. Moreover, restoration of miR-378 could impair the tumor suppression role of downregulated-miR-378 on NSCLC growth.

CONCLUSIONS: Decreased-miR-378 exerted tumor-suppressive effects on NSCLC growth via targeting FOXG1 in vitro, which provided an innovative and candidate target for diagnosis and treatment of NSCLC.

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