Methyltransferase-Like 3 in Gastric Cancer: Advances in Understanding Its Intricate Roles and Therapeutic Implications.

Gastric cancer is a common malignant tumor and a leading cause of cancer-related deaths globally. Recent research has shed light on the impact of N6-methyladenosine (m6A) methylation on the proliferation and metastasis of various malignancies, including gastric cancer. The methyltransferase complex catalyzes m6A methylation, with methyltransferase-like 3 (METTL3) serving as the sole catalytic subunit of m6A. Growing evidence indicates that METTL3 plays a pivotal role in the development and progression of gastric cancer; thus, targeting METTL3 could be a new treatment strategy for gastric cancer. In addition, recent studies have identified a role for METTL3 in the development of drug resistance in gastric cancer. However, these recent advancements have not yet been highlighted. In this review, we synthesized recent studies on the complex role of METTL3 in the pathogenesis and drug resistance of gastric cancer to elucidate the underlying mechanisms involving interplay with coding and noncoding RNAs, both dependent and independent of the methyltransferase activity of METTL3. These findings advance our understanding of METTL3 in gastric cancer, and they also have important clinical implications for the development of novel therapeutic approaches, including targeted and personalized treatment strategies, ultimately improving the management and care of patients with gastric cancer.