Mechanisms of PM2.5 Exposure Impact on the Malignant Progression of Breast Cancer Subtype [MDA-MB-231 RNA-seq]

As a major global health threat to women, breast cancer demonstrates significant molecular subtype-specific variations in response to PM2.5 exposure. While epidemiological evidence has confirmed the association between PM2.5 and breast cancer, the molecular mechanisms by which severe PM2.5 pollution drives subtype heterogeneity remain poorly understood and are difficult to characterize using conventional phenotypic approaches. To address this, we apply integrated transcriptomic sequencing and bioinformatics analysis to investigate molecular response mechanisms in three representative breast cancer cell lines—Luminal A (MCF-7), Luminal B (T-47D), and triple-negative (MDA-MB-231)—following severe PM2.5 exposure. Our results reveal that although all three subtypes share a common response to the stress of metal ions and inorganic substances, each exhibits distinct molecular alterations after PM2.5 exposure: the response mechanisms of MCF-7 cells are primarily involved in extracellular matrix remodeling, neuro-lik differentiation, and inflammatory signaling; T-47D cells show significant enrichment in the synaptic membrane, oxidoreductase metabolism, and ferroptosis pathway; and MDA-MB-231 cells exhibit a core response centered on cell cycle progression and mitosis. Furthermore, we identify subtype-specific hub genes and predict the corresponding targeted drugs: Niclosamide targeting BRCA1 in MCF-7, Menadione targeting NQO1 in T-47D, and PHA-793887 targeting CDK1 in MDA-MB-231. This study establishes a comprehensive research framework spanning environmental exposure, cellular response, clinical validation, and drug prediction. The findings provide important insights into the subtype-specific carcinogenic mechanisms of PM2.5 and support the development of individualized prevention strategies for breast cancer.