ArticleScientific reports2026
Upregulated miR-204-5p inhibits oral squamous cell carcinoma progression via inducing autophagy-promoted apoptosis by targeting PIK3CB.
Article in Scientific reports, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
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.
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