miR‐450b promotes cell migration and invasion by inhibiting SERPINB2 in oral squamous cell carcinoma.

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    • Abstract:
      Objective: microRNA‐450b (miR‐450b) plays an important role in cancer progression; however, its function in oral squamous cell carcinoma (OSCC) remains largely unknown. This study aimed to investigate the action mechanisms of miR‐450b in OSCC. Materials and Methods: OSCC animal model was established via continuous induction with single‐drug 7, 12‐dimethylbenzo[a]anthracene (DMBA). Animal tissue samples were pathologically typed using haematoxylin–eosin (HE) staining. The Cancer Genome Atlas (TCGA) database was used to predict miR‐450b and SERPINB2 expression in head and neck squamous cell carcinoma (HNSCC). qRT‐PCR and Western blotting were used to detect gene and protein expression in OSCC tissue and cells, respectively. OSCC cell proliferation, growth, migration and invasion were detected using CCK‐8, colony formation, transwell migration and matrigel invasion assays, respectively. Bioinformatic tools were used to predict miR‐450b target genes. Dual‐luciferase reporter assay was used to verify targeting between miR‐450b and SERPINB2. Finally, small interfering RNA (siRNA) was used to reduce SERPINB2 expression to detect its effect on tumourigenesis. Results: Four stages of OSCC carcinogenesis (normal oral epithelium, simple epithelial hyperplasia, dysplasia and OSCC) were identified. miR‐450b was found to be overexpressed in OSCC animal samples, HNSCC samples and human OSCC cells. Upregulation of miR‐450b significantly promoted OSCC cell proliferation, colony formation, migration and invasion, while its downregulation had the opposite effect. SERPINB2 was found to be a miR‐450b target gene, and its expression was negatively correlated with miR‐450b expression. Altering SERPINB2 expression effectively inhibited OSCC cell invasion, metastasis and epithelial‐mesenchymal transition (EMT). Conclusions: miR‐450b plays a key role in OSCC tumourigenesis by regulating OSCC cell migration, invasion and EMT via SERPINB2. [ABSTRACT FROM AUTHOR]
    • Abstract:
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