METTL3 in esophageal cancer: Current insights into molecular mechanisms, subtype heterogeneity and targeted therapy prospects (Review)

A‑independent functions or direct immune‑checkpoint regulation remain unvalidated in EC. Crucially, METTL3 actively modulates DNA damage repair and radiotherapy resistance, exposing a promising therapeutic vulnerability, although clinical pharmacological development remains nascent. Furthermore, METTL3 biology in EAC remains conspicuously uncharacterized. By strictly stratifying evidence by EC subtype, the present review distinguishes empirically validated mechanisms from premature cross‑cancer extrapolations. Ultimately, a novel conceptual framework that redefines METTL3 not merely as a static oncogene, but as a dynamic, context‑dependent regulatory hub, is proposed. Under therapeutic stress, METTL3 amplifies cellular phenotypic plasticity, systematically orchestrating tumor adaptation and treatment resistance.