Phthalates unleashed: decoding ovarian carcinogenesis through multi-omics networks, single-cell insights, and molecular docking

Abstract Background Despite epidemiological studies linking phthalates to ovarian cancer, their multi-target molecular mechanisms remain unresolved, hindering biomarker discovery and preventive strategies. This study integrates network toxicology, multi-omics analyses, and molecular docking to syste...

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Main Authors: Junchan Yang, Min Luo, Hongjun Wang, Jinfa Huang
Format: Article
Language:English
Published: BMC 2025-06-01
Series:Journal of Ovarian Research
Subjects:
Online Access:https://doi.org/10.1186/s13048-025-01710-6
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author Junchan Yang
Min Luo
Hongjun Wang
Jinfa Huang
author_facet Junchan Yang
Min Luo
Hongjun Wang
Jinfa Huang
author_sort Junchan Yang
collection DOAJ
description Abstract Background Despite epidemiological studies linking phthalates to ovarian cancer, their multi-target molecular mechanisms remain unresolved, hindering biomarker discovery and preventive strategies. This study integrates network toxicology, multi-omics analyses, and molecular docking to systematically delineate phthalate-driven oncogenic pathways, thereby bridging mechanistic gaps and informing targeted interventions. Results We identified 234 potential targets related to phthalate exposure and ovarian cancer. Enrichment analysis revealed that these genes are associated with HIF-1 signaling, and metabolic pathways that promote cancer progression. Seven core genes were identified, with six (GAPDH, CASP3, PPARG, ESR1, CYCS, SIRT1, and CCND1) exhibiting differential expression in the TCGA ovarian cancer cohort. Single-cell analysis confirmed their widespread expression across various cell types, underscoring their roles in tumor biology. Molecular docking revealed specific binding interactions between phthalates and six core proteins. Conclusions Integrated computational analyses indicate that phthalates (DEP, DMP, DOP) may drive ovarian carcinogenesis through metabolic reprogramming (HIF-1α/glycolysis), strong binding to SIRT1/PPARα regulators, and tumor microenvironment remodeling. These findings establish a framework for prioritizing environmental carcinogens and identifying exposure biomarkers, with implications for reevaluating phthalate safety and elucidating the SIRT1-HIF1-PPARα axis in cancer pathogenesis.
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spelling doaj-art-fe5ae80b020a487eb20eb950662c99fb2025-08-20T02:40:15ZengBMCJournal of Ovarian Research1757-22152025-06-0118111410.1186/s13048-025-01710-6Phthalates unleashed: decoding ovarian carcinogenesis through multi-omics networks, single-cell insights, and molecular dockingJunchan Yang0Min Luo1Hongjun Wang2Jinfa Huang3Department of Gynecology, The Eighth Affiliated Hospital, Southern Medical University (The First People’s Hospital of Shunde, Foshan)Department of Gynecology, The Eighth Affiliated Hospital, Southern Medical University (The First People’s Hospital of Shunde, Foshan)Department of Gynecology, The Eighth Affiliated Hospital, Southern Medical University (The First People’s Hospital of Shunde, Foshan)Department of Gynecology, The Eighth Affiliated Hospital, Southern Medical University (The First People’s Hospital of Shunde, Foshan)Abstract Background Despite epidemiological studies linking phthalates to ovarian cancer, their multi-target molecular mechanisms remain unresolved, hindering biomarker discovery and preventive strategies. This study integrates network toxicology, multi-omics analyses, and molecular docking to systematically delineate phthalate-driven oncogenic pathways, thereby bridging mechanistic gaps and informing targeted interventions. Results We identified 234 potential targets related to phthalate exposure and ovarian cancer. Enrichment analysis revealed that these genes are associated with HIF-1 signaling, and metabolic pathways that promote cancer progression. Seven core genes were identified, with six (GAPDH, CASP3, PPARG, ESR1, CYCS, SIRT1, and CCND1) exhibiting differential expression in the TCGA ovarian cancer cohort. Single-cell analysis confirmed their widespread expression across various cell types, underscoring their roles in tumor biology. Molecular docking revealed specific binding interactions between phthalates and six core proteins. Conclusions Integrated computational analyses indicate that phthalates (DEP, DMP, DOP) may drive ovarian carcinogenesis through metabolic reprogramming (HIF-1α/glycolysis), strong binding to SIRT1/PPARα regulators, and tumor microenvironment remodeling. These findings establish a framework for prioritizing environmental carcinogens and identifying exposure biomarkers, with implications for reevaluating phthalate safety and elucidating the SIRT1-HIF1-PPARα axis in cancer pathogenesis.https://doi.org/10.1186/s13048-025-01710-6PhthalatesMolecular dockingScCancerExplorerOvarian cancerNetwork toxicology
spellingShingle Junchan Yang
Min Luo
Hongjun Wang
Jinfa Huang
Phthalates unleashed: decoding ovarian carcinogenesis through multi-omics networks, single-cell insights, and molecular docking
Journal of Ovarian Research
Phthalates
Molecular docking
ScCancerExplorer
Ovarian cancer
Network toxicology
title Phthalates unleashed: decoding ovarian carcinogenesis through multi-omics networks, single-cell insights, and molecular docking
title_full Phthalates unleashed: decoding ovarian carcinogenesis through multi-omics networks, single-cell insights, and molecular docking
title_fullStr Phthalates unleashed: decoding ovarian carcinogenesis through multi-omics networks, single-cell insights, and molecular docking
title_full_unstemmed Phthalates unleashed: decoding ovarian carcinogenesis through multi-omics networks, single-cell insights, and molecular docking
title_short Phthalates unleashed: decoding ovarian carcinogenesis through multi-omics networks, single-cell insights, and molecular docking
title_sort phthalates unleashed decoding ovarian carcinogenesis through multi omics networks single cell insights and molecular docking
topic Phthalates
Molecular docking
ScCancerExplorer
Ovarian cancer
Network toxicology
url https://doi.org/10.1186/s13048-025-01710-6
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