[Clinical significance and molecular mechanisms of m⁶A modification in oral squamous cell carcinoma]

Oral squamous cell carcinoma (OSCC) represents the most prevalent primary malignant neoplasm within the head and neck region. The elevated rates of recurrence and metastasis, coupled with resistance to conventional therapies, significantly compromise patient prognosis, thereby necessitating the identification of novel molecular regulatory targets. N⁶-methyladenosine (m⁶A) modification emerges as the most widespread post-transcriptional RNA modification in eukaryotic organisms. This modification operates through a dynamic regulatory network involving methyltransferases (Writers), demethylases (Erasers), and recognition proteins (Readers), which collectively orchestrate precise regulation of RNA functionality and are intricately involved in oncogenic processes. Current research indicates that m⁶A modification and its associated regulatory factors exhibit aberrant dysregulation in OSCC. By modulating critical biological processes such as tumor cell proliferation, invasion, metastasis, autophagy, ferroptosis, and the characteristics of OSCC tumor stem cells, these modifications influence both the progression and therapeutic responsiveness of OSCC. This article systematically reviews the core regulatory mechanisms of m⁶A modification, focusing on its functional effects and molecular pathways in the malignant progression of OSCC. It summarizes the clinical translational value of m⁶A regulatory factors as diagnostic and prognostic biomarkers as well as targets for targeted therapy, and outlines future research directions in this field, aiming to provide important theoretical references for the precision diagnosis and treatment of OSCC.