Unlocking the role of miR-17: Driving G1-S cell cycle transition in oral tongue cancer through integrated bioinformatics and laboratory analyses.

Abstract

Objective: This study aims to identify miRNA-mediated regulation of the cell cycle in oral tongue cancer.

Methods: Comprehensive computational analysis was performed on the GEO dataset "GSE168227". DIANA Tool-mir path v.3, STRING, Cytoscape 3.6.0, Enrichr, and TargetScan Human 7.2 were utilized to identify and analyze miRNAs and their targets in oral tongue cancer. The identified miRNA and its target genes were further analyzed in oral tongue cancer patients using qPCR and immunohistochemistry (IHC).

Results: Computational analysis revealed miR-17 as a differentially expressed miRNA in oral tongue cancer. Database analysis indicated potential binding sites of miR-17 for CDKN1A and CCND1 mRNA at 3'-UTR. In oral tongue cancer samples, miR-17, CDKN1A, and CCND1expression were upregulated compared to controls. IHC demonstrated overexpression of p21 and Cyclin D1 across various tumor grades, with predominant cytoplasmic expression of p21 observed in oral tongue cancer samples.

Conclusion: The findings suggest that miR-17 may regulate the G1-S transition of the cell cycle in oral tongue cancer. Further validation and functional studies are warranted to confirm their role as biomarkers.