Upregulated miR-204-5p inhibits oral squamous cell carcinoma progression via inducing autophagy-promoted apoptosis by targeting PIK3CB

In the present work, qRT-PCR was used to detect miR-204-5p level in the normal oral epithelial cells (HaCat cell line) and OSCC cells (SCC-15 and SCC-25 cell lines). We explored the impact of miR-204-5p on OSCC through overexpression of miR-204-5p in OSCC cells by transient transfection. CCK-8, EdU, and clone formation assays were applied to estimate how miR-204-5p acts on OSCC proliferation in vitro. Wound healing and transwell assays were performed to evaluate the in vitro effect of miR-204-5p on OSCC migration. Flow cytometry, Dual luciferase report assay and western blotting were used to explore the mechanism. The in vivo effect of miR-204-5p was evaluated by xenograft models. Compared with normal cells, OSCC cells showed lower expression levels of miR-204-5p. miR-204-5p was evidently elevated in OSCC after transfection. In CCK-8, clone formation and Edu assays, miR-204-5p inhibited OSCC proliferation. Meanwhile, miR-204-5p attenuated OSCC migration in wound healing and transwell assays. Moreover, The levels of N-cadherin, E-cadherin, and vimentin were lowered. In flow cytometry and western blotting, miR-204-5p promoted the apoptosis rate and decreased Bcl-2/Bax ratio. Moreover, elevated LC3-Ⅱ/LC3-Ⅰ ratio suggested miR-204-5p induced autophagy in OSCC. Interestingly, autophagy inhibitor 3-MA partially restored the OSCC’s resistance to apoptosis. Further, miR-204-5p inactivated the PI3K/Akt/mTOR pathway, whereas dual luciferase assay demonstrated PIK3CB was a direct target of miR-204-5p. In vivo, miR-204-5p hindered OSCC growth. This study demonstrated that miR-204-5p inhibited OSCC progression through inducing autophagy-promoted apoptosis by targeting PIK3CB.