ArticleFrontiers in pharmacology2026
Integrative network toxicology and molecular docking reveal epigenetic and endocrine-disrupting mechanisms of PFAS in ovarian cancer.
Article in Frontiers in pharmacology, 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Per- and polyfluoroalkyl substances (PFAS) are omnipresent, persistent contaminants associated with rising ovarian cancer incidence; however, the molecular circuitry linking PFAS to ovarian tumorigenesis remains obscure. Methods: Here, an integrated network toxicology-molecular docking pipeline was developed to interrogate ten environmentally abundant PFAS. Results: Comprehensive interactome mapping identified 1,042 PFAS-protein interactions that converge on eight transcriptional hubs (HDAC1, SIRT1, ESR1, RXRA, PTGS2, MMP9, HDAC2 and HDAC3), subsequently validated as significantly overexpressed in ovarian tumours versus normal tissue pathway enrichment indicated that these mediators synchronize epigenetic silencing, estrogen signalling, inflammatory prostaglandin synthesis and extracellular-matrix remodelling, thereby may coordinate processes potentially associated with PFAS-associated initiation and progression. Competitive docking further showed that long-chain PFOS and PFOA are predicted the strongest binding affinities to the catalytic domains of HDACs 1-3, mechanistically explaining the observed transcriptomic alterations. Human ovarian granulosa-like tumor cell line (KGN) was exposed to PFOA, which works as a representative PFAS compound, showed a significant increase of cell proliferation and migration, leading to an alteration of gene expression previously identified by network toxicology. Discussion: Our findings provides a systems-level predictive framework for understanding PFAS-associated ovarian oncogenesis, furnish quantitative biomarkers for exposure-response modelling, and prioritize HDAC inhibition as prioritized candidate mediators to mitigate PFAS-related cancer risk with immediate translational implications for public-health protection and regulatory guideline revision.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.