ArticleMedicine2025
Molecular mechanism of bisphenol A in promoting esophageal carcinoma based on network toxicology and molecular docking.
Article in Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
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Who cites it
1 citing paper in PubMed.
- Integrating Network Toxicology with Molecular Dynamics Simulations to Reveal Key Targets and Binding Mechanisms of Bisphenol A in Pancreatic Ductal Adenocarcinoma.International journal of molecular sciences · 2026Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bisphenol A (BPA) is a pervasive endocrine-disrupting chemical with estrogenic activity and has been implicated in the development of multiple malignancies. However, its molecular mechanisms in esophageal carcinoma (ESCA) remain unclear. This study aimed to elucidate the potential oncogenic pathways through which BPA contributes to ESCA progression. Network toxicology was applied to collect BPA-related targets and ESCA-associated genes from multiple public databases. Overlapping targets were identified for further protein-protein interaction (PPI) and enrichment analyses to investigate functional pathways. Molecular docking was performed to assess binding affinities between BPA and core targets. The Cancer Genome Atlas (TCGA) was used for expression and survival validation, while mutation profiles were examined via cBioPortal. A total of 100 BPA-related targets and nearly 50,000 ESCA-associated genes were retrieved, yielding 95 overlapping targets. PPI network analysis and enrichment results highlighted HSP90AA1 and HSP90AB1 as central hub genes associated with protein kinase regulation, telomerase activity, and immune-inflammatory signaling pathways. Molecular docking confirmed strong binding affinities between BPA and HSP90AA1/HSP90AB1 (-7.5 and -7.0 kcal/mol, respectively). TCGA analyses showed that both genes were significantly upregulated in ESCA tissues, and high expression correlated with poorer overall survival. Mutation profiling indicated that HSP90AB1 exhibited a higher alteration frequency (13%), predominantly driven by gene amplification. This integrative multi-omics analysis provides compelling evidence that BPA may facilitate ESCA progression through HSP90AA1/HSP90AB1-mediated oncogenic and immune-inflammatory pathways. These findings deepen understanding of environmental carcinogenesis and suggest potential molecular targets for ESCA prevention and treatment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.