Switching from messenger RNAs to noncoding RNAs, METTL3 is a novel colorectal cancer diagnosis and treatment target

N6-methyladenosine (m6A) modification, one of the most prevalent RNA epigenetic modifications in eukaryotes, constitutes over 60% of all RNA methylation modifications. This dynamic modification regulates RNA processing, maturation, nucleocytoplasmic transport, translation efficiency, phase separation, and stability, thereby linking its dysregulation to diverse physiological and pathological processes. METTL3, a core catalytic component of the methyltransferase complex responsible for m6A deposition, is frequently dysregulated in diseases, including colorectal cancer (CRC). Although METTL3's involvement in CRC pathogenesis has been documented, its precise molecular mechanisms and functional roles remain incompletely understood. METTL3 mediates CRC progression-encompassing proliferation, invasion, drug resistance, and metabolic reprogramming-through m6A-dependent modulation of both coding RNAs and noncoding RNAs. Its regulatory effects are primarily attributed to interactions with key signaling pathways at multiple stages of CRC development. Emerging evidence highlights METTL3 as a promising biomarker for CRC diagnosis and prognosis, as well as a potential therapeutic target. By synthesizing recent advances in METTL3 research within CRC, this review provides critical insights into novel strategies for clinical diagnosis and targeted therapy.