TARGETING WNT PATHWAY THROUGH miR-142-3P AS A POTENTIAL THERAPEUTIC APPROACH IN ORAL SQUAMOUS CELL CARCINOMA (IN VITRO STUDY)

INTRODUCTION: Oral squamous cell carcinoma (OSCC) accounts for 95% of oral cancers and is associated with a low 5-year survival rate using the conventional treatments methods. Advancements in oncological research require understanding the molecular mechanisms driving OSCC occurrence and progression to devise more effective therapeutic approaches and improving prognostic outcomes. Among these mechanisms, the WNT/β -catenin signaling pathway is recognized for its contribution in promoting tumorigenesis, cancer progression, and metastasis, making it a potential target for unconventional cancer therapies. MicroRNA-142-3p (miR-142-3p), a constituent of the miR-142 family, has demonstrated tumor-suppressive properties in certain malignancies. It was proposed that miR-142-3p positively modulates WNT signaling by directly targeting the adenomatous polyposis coli (APC) gene. This targeting destabilizes β -catenin, resulting in suppression of WNT pathway activity. OBJECTIVES: In this current investigation, the aim was to explore the capabilities of miR-142-3p in modulating the WNT pathway and evaluating its impact on the proliferation, migration, and apoptosis of OSCC-4 cells. METHODOLOGY: MiR-142-3p was transfected into OSCC-4 cell line. MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide) assay was employed to determine cytotoxicity, while the impact on cell migration was evaluated through scratch wound healing test. Apoptotic effects were evaluated using Annexin-V, while cell proliferation was measured through Ki-67 staining, both analyzed by flow cytometry. RESULTS: The results indicated that miR-142-3p suppressed OSCC-4 proliferation and migration, demonstrating its anti-proliferative potential. It didn't induce early apoptosis however, it enhanced late-stage apoptosis in a dose-dependent manner. CONCLUSIONS: miR-142-3p exhibits a promise as a potential therapeutic option for OSCCs.