Effects and mechanisms of N6-methyladenosine RNA methylation in environmental pollutant-induced carcinogenesis.

Environmental pollution, including air pollution, plastic contamination, and heavy metal exposure, is a pressing global issue. This crisis contributes significantly to pollution-related diseases and is a critical risk factor for chronic health conditions, including cancer. Mounting evidence underscores the pivotal role of N6-methyladenosine (m6 A) as a crucial regulatory mechanism in pathological processes and cancer progression. Governed by m6 A writers, erasers, and readers, m6 A orchestrates alterations in target gene expression, consequently playing a vital role in a spectrum of RNA processes, covering mRNA processing, translation, degradation, splicing, nuclear export, and folding. Thus, there is a growing need to pinpoint specific m6 A-regulated targets in environmental pollutant-induced carcinogenesis, an emerging area of research in cancer prevention. This review consolidates the understanding of m6 A modification in environmental pollutant-induced tumorigenesis, explicitly examining its implications in lung, skin, and bladder cancer. We also investigate the biological mechanisms that underlie carcinogenesis originating from pollution. Specific m6 A methylation pathways, such as the HIF1A/METTL3/IGF2BP3/BIRC5 network, METTL3/YTHDF1-mediated m6 A modification of IL 24, METTL3/YTHDF2 dynamically catalyzed m6 A modification of AKT1, METTL3-mediated m6 A-modified oxidative stress, METTL16-mediated m6 A modification, site-specific ATG13 methylation-mediated autophagy, and the role of m6 A in up-regulating ribosome biogenesis, all come into play in this intricate process. Furthermore, we discuss the direction regarding the interplay between pollutants and RNA metabolism, particularly in immune response, providing new information on RNA modifications for future exploration.