ArticleACS omega2026
Deciphering the Effect of Methyl 4‑Hydroxybenzoate on Breast Cancer by Bioinformatics and Experiments.
Article in ACS omega, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
0 citing papers in PubMed.
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Methyl 4-hydroxybenzoate (MEP), a widespread environmental contaminant, is suspected to increase breast cancer (BRCA) risk; however, its molecular mechanism remains unclear. Using public health databases, we performed differential expression analysis, network toxicology modeling, and protein-protein interaction mapping to identify candidate biomarkers. Functional interrogation using gene set enrichment analysis, immune infiltration profiling, and molecular docking elucidated the mechanistic roles of these genes in BRCA. Single-cell transcriptomic analysis highlighted the cell populations most relevant to tumor initiation and tracked the biomarker expression patterns within these populations. Subsequently, in vitro assays revealed the direct effects of MEP on malignant behavior. CCNE1, CDK1, E2F1, and EZH2 emerged as core drivers converging on multiple oncogenic pathways. Fifteen immune cell subsets showed markedly altered infiltration patterns in tumors, with macrophages and related populations associated with disease progression. Among the identified biomarkers, CCNE1 exhibited the strongest predicted affinity for MEP (-6.2 kcal mol
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Registered trials
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