Abstract

Objective(s) The research aimed to investigate the impact of hsa-miR-514a-3p on the proliferation and invasion of oral squamous cell carcinoma (OSCC), and to identify its potential target gene COL1A1 . Design The expression patterns, functional enrichment (Gene Set Enrichment Analysis, GSEA), and copy number variations (CNV) of miR-514a-3p and COL1A1 were analyzed using public datasets (E_MTAB_8588, GSE75538, TCGA-HNSC, and Human Protein Atlas, HPA). The expressions of miR-514a-3p and COL1A1 in clinical samples were detected by immunohistochemistry (IHC) and RT-qPCR. Lentiviral vectors (oe- miR-514a-3p , sh- miR-514a-3p , oe- COL1A1 , and sh- COL1A1 ) were transfected into SCC-25 cells. The expressions of COL1A1 , epithelial-mesenchymal transition (EMT)-related molecules, and matrix metalloproteinases ( MMPs ) were detected by RT-qPCR, Western blotting, and ELISA. Cell functions were evaluated using colony formation assay, Transwell assay, flow cytometry, and CCK-8 assay. A dual-luciferase reporter assay was used to verify the binding between miR-514a-3p and COL1A1 . Results Hsa-miR-514a-3p showed a significant downregulation in OSCC tissues compared to adjacent controls. Hsa-miR-514a-3p overexpression led to reduced OSCC cell proliferation and invasion, whereas its downregulation resulted in increased these processes. hsa-miR-514a-3p directly targeted COL1A1 , with negative correlation in OSCC samples. Silencing COL1A1 mimicked the suppressive effects of hsa-miR-514a-3p , and COL1A1 overexpression partially reversed them. Conclusion This study demonstrates that hsa-miR-514a-3p inhibits malignant phenotypes of OSCC cells by targeting COL1A1 , providing insights into potential therapeutic targets for OSCC management.