甲状腺がんにおけるM6Aメチル化：機能、メカニズム、および臨床的意義

Thyroid cancer (TC), the most prevalent endocrine malignancy, exhibits marked biological heterogeneity and a persistent therapeutic gap in aggressive, treatment-refractory subsets. N6-methyladenosine (m6A), pervasive across eukaryotic RNA processing-splicing, maturation, stability, translation, and localization-constitutes a central layer of epigenetic regulation. By reshaping post-transcriptional programs, m6A modifications govern tumor initiation and progression, sustaining stemness, accelerating proliferation and invasion, and mediating therapy resistance. A growing body of evidence implicates dysregulated m6A regulators in TC pathogenesis; yet the multiplicity of effectors and their context-dependent actions complicate mechanistic resolution. This review synthesizes current advances, delineating m6A's involvement in four cardinal arenas of thyroid tumorigenesis: altered cellular behaviors (proliferation, migration), metabolic reprogramming, programmed cell death (apoptosis and ferroptosis), and resistance to targeted, radioactive iodine, and immunotherapeutic strategies. We further examine the emerging interface between m6A and non-coding RNAs, highlighting how this axis rewires oncogenic networks. Finally, we appraise the translational potential of m6A as a diagnostic and prognostic biomarker and as a therapeutic target, offering perspective on opportunities and challenges for epitranscriptome-guided precision oncology in TC.