环境污染,包括空气污染,塑料污染,和重金属暴露,是一个紧迫的全球性问题。这场危机极大地助长了与污染有关的疾病,并且是慢性健康状况的关键风险因素,包括癌症.越来越多的证据强调了N6-甲基腺苷(m6A)作为病理过程和癌症进展中的关键调节机制的关键作用。由M6A作家管理,橡皮擦,和读者,m6A协调靶基因表达的改变,因此在一系列RNA过程中起着至关重要的作用,涵盖mRNA加工,翻译,降解,拼接,核出口,和折叠。因此,越来越需要在环境污染物诱导的致癌作用中确定特定的m6A调节目标,癌症预防研究的新兴领域。这篇综述巩固了对环境污染物诱导的肿瘤发生中m6A修饰的理解,明确检查它在肺部的影响,皮肤,和膀胱癌。我们还研究了源自污染的致癌作用的生物学机制。特定的m6A甲基化途径,如HIF1A/METTL3/IGF2BP3/BIRC5网络,METTL3/YTHDF1介导的IL24的m6A修饰,METTL3/YTHDF2动态催化的AKT1的m6A修饰,METTL3介导的m6A修饰的氧化应激,METTL16介导的m6A修饰,位点特异性ATG13甲基化介导的自噬,以及m6A在上调核糖体生物发生中的作用,都在这个复杂的过程中发挥作用。此外,我们讨论了污染物和RNA代谢相互作用的方向,特别是在免疫反应中,为将来的探索提供有关RNA修饰的新信息。
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 (m6A) as a crucial regulatory mechanism in pathological processes and cancer progression. Governed by m6A writers, erasers, and readers, m6A 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 m6A-regulated targets in environmental pollutant-induced carcinogenesis, an emerging area of research in cancer prevention. This review consolidates the understanding of m6A 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 m6A methylation pathways, such as the HIF1A/METTL3/IGF2BP3/BIRC5 network, METTL3/YTHDF1-mediated m6A modification of IL 24, METTL3/YTHDF2 dynamically catalyzed m6A modification of AKT1, METTL3-mediated m6A-modified oxidative stress, METTL16-mediated m6A modification, site-specific ATG13 methylation-mediated autophagy, and the role of m6A 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.