Abstract

Introduction: Oral squamous cell carcinoma (OSCC) accounts for 90 % of oral malignancies and is associated with a 5-year mortality rate of 40–50 % worldwide. Despite advances in surgery, radiotherapy, and systemic chemotherapy, therapeutic outcomes remain unsatisfactory because of the tumour’s complex molecular landscape and substantial genetic heterogeneity. This study focuses on the MYC (Myelocytomatosis) proto-oncogene, a master regulator of cell proliferation, metabolism and apoptosis that plays a pivotal role in OSCC pathogenesis. Aberrant MYC overexpression drives uncontrolled cellular proliferation, genomic instability, and resistance to conventional therapies. Given that MYC is widely considered ‘undruggable’, indirect strategies that disrupt MYC-associated signalling pathways are urgently required.

Methods: We investigated whether microRNAs (miRNAs) can modulate MYC expression. In silico screening of miRDB, miRBase and complementary repositories identified miR-204-3p as a putative tumour suppressor. Bioinformatic prediction suggested that miR-204-3p targets the 3′-untranslated regions of MYC and its functional partners (MAX, MAZ, MYCL), thereby attenuating MYC signalling.

Results: Transcriptomic analysis of OSCC tissues demonstrated significant upregulation of MYC relative to matched normal mucosa (p < 0.01). Conversely, miR-204-3p expression was markedly reduced, corroborating its putative role as an endogenous MYC antagonist.

Conclusion: These findings implicate the MYC–miR-204-3p axis as a tractable therapeutic vulnerability in OSCC. Restoration of miR-204-3p may suppress MYC-driven tumour progression and improve the efficacy of existing treatment modalities. Future studies could facilitate the development of innovative diagnostic assays and targeted miRNA-based therapies, ultimately enhancing patient outcomes. This work underscores the importance of miRNA research in elucidating cancer biology and paves the way for novel therapeutic strategies in OSCC management.