ArticleDiscover oncology2026
Integrated network toxicology and immune profiling identify ESR1 as a potential hub linking Benzo[a]pyrene exposure to gastric cancer risk.
Article in Discover oncology, 2026. 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
objectiveTo elucidate the molecular mechanisms of Benzo[a]pyrene (BaP)-induced gastric cancer (GC) and identify core regulatory targets as potential biomarkers for GC.
methodsThe chemical structure and physicochemical properties of BaP were obtained from PubChem, ProTox, and ChEMBL databases, along with its active targets. GC-related pathogenic targets were retrieved from GeneCards, OMIM, and TTD. Intersecting targets between BaP and GC were identified, and a "BaP-intersecting targets-GC" ternary regulatory network was constructed. Functional enrichment analysis was performed on the intersecting targets, and a protein-protein interaction (PPI) network was built. Core targets were screened using the Degree algorithm, and their expression differences in GC were validated. The prognostic value of these targets was assessed using Kaplan-Meier survival curves. Immunofluorescence was used to determine the subcellular localization of core targets, and their roles in immune infiltration and genetic mutations were preliminarily explored. Finally, molecular docking was employed to reveal the potential interaction between BaP and core targets at the molecular structural level.
resultsA total of 292 BaP-active targets and 1,214 GC-related targets were identified, with 28 overlapping targets. Functional enrichment analysis revealed that these intersecting targets were associated with biological processes or signaling pathways such as protein autophosphorylation, insulin-like growth factor receptor binding, and the Ras signaling pathway. ESR1, INS, and CDK2 were central nodes in the PPI network, with ESR1 being the most critical core regulatory target (Degree = 17). Expression analysis showed that ESR1 was significantly downregulated in GC (P = 4.3
conclusionIn conclusion, our integrated computational study provides preliminary evidence suggesting ESR1 as a potential hub linking BaP exposure to gastric cancer risk, possibly via influencing immune features. This identifies ESR1 as a candidate biomarker and reveals a testable hypothesis for future mechanistic investigation.
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