Related Experiment Video

Updated: Feb 8, 2026

Collection of Alfalfa Root Exudates to Study the Impact of Di2-ethylhexyl Phthalate on Metabolite Production
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Collection of Alfalfa Root Exudates to Study the Impact of Di2-ethylhexyl Phthalate on Metabolite Production

Published on: June 2, 2023

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Analysis of the molecular mechanism underlying di(2-ethylhexyl) phthalate-induced bladder carcinogenesis via network

Manfei Jiang1, Chuanwei Sun2, Baofeng Wang1

  • 1Department of Urology, The Second Affiliated Hospital of Hainan Medical University, Haikou City, Hainan, China.

Medicine
|February 6, 2026
PubMed

Insights

Di(2-ethylhexyl) phthalate (DEHP) exposure may cause bladder cancer (BLCA) by interacting with key proteins and pathways. This study identifies 7 core targets involved in DEHP-induced BLCA development.

Area of Science:

  • Toxicology
  • Molecular Biology
  • Bioinformatics

Background:

  • Di(2-ethylhexyl) phthalate (DEHP) is a common plasticizer with suspected carcinogenic properties.
  • Understanding the molecular mechanisms of DEHP-induced bladder cancer (BLCA) is crucial for prevention and treatment.

Purpose of the Study:

  • To investigate the toxicity of DEHP and elucidate the molecular mechanisms underlying DEHP-induced BLCA.
  • To identify potential molecular targets and pathways involved in DEHP-induced BLCA using network toxicology and molecular docking.

Main Methods:

  • Network toxicology approaches integrating multiple databases (ChEMBL, STRING, GeneCards, etc.) to identify DEHP targets.
  • Construction of target networks using Cytoscape and analysis of core targets.
  • Gene Ontology and KEGG pathway enrichment analyses.
  • Molecular docking using CB-Dock 2 to validate DEHP-target interactions.

Main Results:

  • 105 potential targets for DEHP-induced BLCA were identified, with 7 core targets selected: CDK1, IL-6, CDK2, CCNB1, ERBB2, CCNB2, and BCL2.
  • Differential expression of core targets was observed in tumor tissues (e.g., IL-6 and BCL2 downregulated; CDK1, CDK2, CCNB1, ERBB2, CCNB2 upregulated).
  • Enrichment analyses revealed involvement in cell signaling and cancer-related pathways. Molecular docking confirmed DEHP interactions with core targets.

Conclusions:

  • DEHP may promote BLCA development through interactions with identified core targets and associated signaling pathways.
  • This study provides a theoretical foundation for understanding DEHP-induced BLCA.
  • The findings offer potential references for future prevention and treatment strategies for DEHP-related bladder cancer.
Keywords:
bladder cancerdata miningdi(2-ethylhexyl) phthalatemolecular dockingnetwork toxicology

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