ArticleDiscover oncology2025
Toxicity and mechanistic analysis of di(2-ethylhexyl)phthalate in renal cell carcinoma progression: a systematic study with network toxicology and molecular docking strategies.
Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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
2 citing papers in PubMed.
- Di(2-Ethylhexyl) Phthalate Exposure and Risk of Diabetic Kidney Disease: Epidemiological Association and Mechanistic Insights.Diabetes/metabolism research and reviews · 2026Article
- Exploring the Toxicological Impact and Mechanisms of DEHP Exposure on Prostate Cancer Through Network Toxicology and Machine Learning Algorithms.Current medicinal chemistry · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Millions of tons of unrecycled plastic pollute landfills and oceans, and di(2-ethylhexyl) phthalate (DEHP), a plasticizer classified as a possible carcinogen, is found in many environments, and poses health risks. Renal cell carcinoma (RCC), one of the most prevalent malignancies, accounted for approximately 434,419 new cases and 155,702 deaths in 2022. DEHP can cause developmental dysregulation, reproductive impairments, tumorigenesis, and transgenerational diseases; however, the mechanisms underlying these effects remain unclear. This study aimed to elucidate the toxic targets and molecular mechanisms associated with DEHP exposure and RCC occurrence by integrating network toxicology and molecular docking, utilizing multilevel bioinformatics data. By systematically utilizing diverse databases, 82 targets associated with both DEHP and RCC were identified. Subsequent screening with STRING and Cytoscape revealed 25 key targets, including CASP3, BCL2, MMP9, BCL2L1, CTSS, and APP. GO and KEGG enrichment analyses revealed that these targets are involved in apoptosis, abnormal hormone activity, cancer-related signaling cascades, ligand-receptor interactions, and endocrine system signaling pathways. Molecular docking simulations via CB-Dock confirmed the high-affinity binding interactions between DEHP and these key targets. These results suggest that DEHP exposure may promote the development of RCC by regulating apoptosis and proliferation through pathways such as neuroactive ligand-receptor interactions, pathways related to cancer, and apoptosis. This study provides a theoretical basis for understanding the molecular mechanisms of DEHP-induced renal carcinogenesis and serves as a foundation for future experimental studies to validate these computational predictions regarding DEHP-associated tumor risk from plastic products and environmental exposure.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.