Role of environmental pollutants in breast cancer: Emphasis on Methyl-4-hydroxybenzoate and Triple-negative breast cancer

Research Hypothesis
We hypothesized that Methyl-4-hydroxybenzoate (MEP), a common preservative and emerging environmental contaminant, contributes to triple-negative breast cancer (TNBC) pathogenesis through specific molecular interactions. A network toxicology framework was employed to systematically investigate MEP exposure and TNBC risk.

Data Contents
This dataset contains supplementary tables supporting the main findings:

Table S1: 561 potential MEP targets from ChEMBL, STITCH-5.0, and SwissTargetPrediction, standardized to gene symbols via UniProt.
Table S2: 2,447 TNBC-associated targets from GeneCards, OMIM, and TTD.
Tables S3–S5: Differentially expressed genes (DEGs) from GSE76250 (GEO) and TCGA datasets, including 319 and 1,442 DEGs respectively, and 192 intersecting TNBC-related DEGs.
Tables S6–S8: WGCNA results identifying TNBC-associated modules (blue from GEO, yellow from TCGA) and 60 key TNBC-related DEGs.
Key Findings
Integrative analysis identified three hub genes (EZH2, NEK2, TYMS) significantly enriched in cancer-related pathways with high diagnostic and prognostic value. These data form the foundation for conclusions that MEP may influence TNBC through these targets.

Data Generation & Usage
MEP targets were predicted using ChEMBL, STITCH, and SwissTargetPrediction. TNBC targets were retrieved from GeneCards, OMIM, and TTD. Transcriptomic data from GEO and TCGA underwent differential expression analysis (limma/DESeq2) with thresholds of adjusted P < 0.05 and |log₂FC| > 1 (GEO) or > 2 (TCGA). WGCNA was performed to identify co-expression modules. Researchers can use these files for replication, extended analyses, pathway enrichment, or meta-analyses. Data are provided in tab-delimited format compatible with standard bioinformatics tools.