[Role of m6A methylation modification in photoaging and ultraviolet-induced skin cancers]

Ultraviolet (UV) radiation, one of the critical environmental carcinogenic factors, promotes skin photoaging and carcinogenesis by inducing DNA damage, oxidative stress, and chronic inflammatory cascades. N6-methyladenosine (m6A)-modifying enzymes (writers, erasers, and readers) play bidirectional regulatory roles in UV-mediated skin pathology. In photoaging, the reactive oxygen species (ROS)-m6A axis accelerates collagen degradation and epithelial-mesenchymal transition (EMT) through modulation of matrix metalloproteinases (MMPs), inflammatory mediators, DNA damage repair, apoptosis, and collagen metabolism. In skin cancers, m6A regulators promote tumor progression by influencing oncogenic signaling, proliferation, invasion, metastasis, and immune evasion. Bioactive monomeric compounds derived from traditional Chinese medicine, including polyphenols, saponins, and alkaloids, can regulate the activity of m6A enzymes to interfere with photoaging and UV-induced skin carcinogenesis. This study integrates current evidence to establish an m6A-targeted epigenetic intervention framework for UV-induced skin injury and highlights the potential of synergistic multi-component m6A-modulating therapeutic strategies as a future research priority.