ArticleToxics2025
Effects of Benzo[a]Pyrene Exposure on Lung Cancer: A Mechanistic Study of Epigenetic m6A Levels and YTHDF1.
Article in Toxics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Benzo[a]pyrene, as the primary component of air pollutants, has been implicated in the pathogenesis of non-small-cell lung cancer (NSCLC). As an m6A reader that facilitates mRNA translation, YTHDF1 serves as a crucial regulator in tumor progression. Therefore, we established Benzo[a]pyrene(B[a]P)-induced bronchial epithelial malignant transformed cells (HBE-P35) to simulate the precancerous lesions of NSCLC and investigated the regulatory axis of YTHDF1 in both HBE-P35 and A549 lung cancer cells. A high level of m6A expression was detected in both HBE-P35 and A549 cells. Over-expression of YTHDF1 was observed in NSCLC tissues and correlated with poor overall survival in NSCLC patients. TMT labeling-based proteomic analysis and clinical lung tissue microarray assays demonstrated that CDK6 and MAP3K6 were positively correlated with YTHDF1 expression. MeRIP and RIP analyses revealed that YTHDF1 mediates the m6A-dependent regulation of CDK6 and MAP3K6 protein expression. The acquisition and deletion of miR-139/145-5p, along with luciferase reporter gene assays, demonstrated that miR-139-5p can target YTHDF1. Therefore, we conclude that YTHDF1 regulates CDK6 and MAP3K6 through m6A in B[a]P-induced HBE-P35 and A549 cells, providing a potential target for lung cancer treatment.
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