ArticlePloS one2026
Integrated computational analysis prioritizes candidate targets and pathways linking ochratoxin A exposure to hepatocellular carcinoma.
Article in PloS one, 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
Ochratoxin A (OTA), a food-borne mycotoxin, has been implicated in hepatotoxicity and potential carcinogenic processes, yet the molecular links between OTA exposure and hepatocellular carcinoma (HCC) remain incompletely understood. This study used an integrated computational workflow to prioritize candidate targets and pathways potentially linking OTA exposure with HCC. OTA-related and HCC-related targets were collected from public databases, intersected, and subjected to functional enrichment analysis. Transcriptomic data from the GSE36376 discovery dataset were analyzed to identify differentially expressed genes, followed by LASSO and SVM-RFE feature selection, immune-cell deconvolution, molecular docking, and molecular dynamics simulation. A total of 214 overlapping OTA-HCC-associated targets were identified and were enriched in pathways related to signal transduction, apoptosis, metabolism, and immune regulation. In GSE36376, 443 differentially expressed genes were identified using p < 0.05 and |log2 fold change| > 1, and overlap analysis yielded 13 shared target genes. Five candidate targets, CYP3A4, KIFC1, AKR1C3, CA2, and TTR, were further prioritized. KIFC1 and AKR1C3 were upregulated in HCC samples, whereas CYP3A4, CA2, and TTR were downregulated. These genes showed apparent discriminatory ability within the discovery dataset, with AUC values ranging from 0.866 to 0.958. Molecular docking predicted favorable OTA-target interactions, with docking energies ranging from -7.4 to -10.8 kcal/mol. CYP3A4 showed the lowest predicted docking energy (-10.8 kcal/mol) and was further evaluated by molecular dynamics simulation, with a protein-fitted OTA RMSD of 1.435 ± 0.097 nm and complex Rg of 2.308 ± 0.010 nm during the equilibrated 20-100 ns trajectory. Overall, this study provides a reproducible hypothesis-generating framework for exploring potential metabolic, genomic-instability-related, and immune-microenvironment links between OTA exposure and HCC. Future validation in independent datasets and experimental models will be important to further assess the biological relevance of these candidate targets and pathways.
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