The Mechanism and Latest Progress of m6A Methylation in the Progression of Pancreatic Cancer

Pancreatic cancer (PC), known as the "king of cancers," is characterized by an exceptionally low five-year survival rate, posing a formidable challenge to global public health. N6-methyladenosine (m6A) methylation is prevalent across various stages of eukaryotic RNA expression, including splicing, maturation, stability, translation, and localization, and represents a pivotal mechanism of epigenetic regulation. m6A methylation influences tumor initiation and progression by modulating post-transcriptional processes, playing a critical role in sustaining cancer cell stemness, promoting cell proliferation, and mediating drug resistance. Extensive research underscores the substantial contribution of m6A modifications to PC development. However, the multiplicity of m6A regulators and their intricate mechanisms of action complicate the landscape. This review aims to deepen the understanding of m6A's role in PC by delineating its involvement in four key areas of tumorigenesis: the hypoxic tumor microenvironment, metabolic reprogramming, immune microenvironment, and resistance mechanisms. Additionally, the review addresses the emerging frontier of m6A interactions with non-coding RNAs (ncRNAs), offering insights into the potential therapeutic and prognostic applications of m6A in the treatment and prognosis prediction of PC.