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Objective <p>To investigate the effects of 1,4-dichlorobenzene (1,4-DCB) on lung adenocarcinoma (LUAD) and elucidate its potential molecular mechanisms, thereby providing a basis for related LUAD risk assessment and intervention.</p> Methods <p>An integrated pipeline combined network toxicology, molecular docking, and immune multi-omics. After retrieving 1,4-DCB–LUAD intersection targets from multiple public repositories, a protein–protein-interaction network was constructed and pruned with TCGA data to identify core targets. Binding affinities were validated by molecular docking. Expression, prognostic value, and immune infiltration patterns of the core targets were subsequently analyzed. Simultaneously, 1,4-DCB toxicity was characterised and a residential exposure inventory was developed.</p> Results <p>1,4-DCB exhibits moderate acute toxicity (LD50 = 500&#xa0;mg/kg) and clear carcinogenic potential. The study identified 40 cross-target interactions and 8 core targets. MMP13 (− 5.7&#xa0;kcal/mol) and CYP1A1 (− 6.7&#xa0;kcal/mol) demonstrated the strongest binding affinities. MMP13 is overexpressed in lung adenocarcinoma, promoting tumor progression. Associated genes are enriched in extracellular matrix remodeling, inflammatory signaling, and the PI3K-Akt pathway. Conversely, CYP1A1 is downregulated and exhibits tumor-suppressive effects, with its interaction network enriched in cytochrome P450-mediated drug metabolism pathways.</p> Conclusion <p>1,4-DCB may participate in the pathogenesis of LUAD through multiple pathways by interacting with MMP13 and CYP1A1, providing scientific basis for risk assessment, diagnosis, and intervention in LUAD.</p> Graphical Abstract <p></p>

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Systemic analysis of 1,4-dichlorobenzenes effects on lung adenocarcinoma environmental exposure and core target regulation prediction

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年1月27日

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  • Bingfeng Ma,
  • Juan Hu,
  • Dingfei Ren,
  • Xuansheng Ding

摘要

Objective

To investigate the effects of 1,4-dichlorobenzene (1,4-DCB) on lung adenocarcinoma (LUAD) and elucidate its potential molecular mechanisms, thereby providing a basis for related LUAD risk assessment and intervention.

Methods

An integrated pipeline combined network toxicology, molecular docking, and immune multi-omics. After retrieving 1,4-DCB–LUAD intersection targets from multiple public repositories, a protein–protein-interaction network was constructed and pruned with TCGA data to identify core targets. Binding affinities were validated by molecular docking. Expression, prognostic value, and immune infiltration patterns of the core targets were subsequently analyzed. Simultaneously, 1,4-DCB toxicity was characterised and a residential exposure inventory was developed.

Results

1,4-DCB exhibits moderate acute toxicity (LD50 = 500 mg/kg) and clear carcinogenic potential. The study identified 40 cross-target interactions and 8 core targets. MMP13 (− 5.7 kcal/mol) and CYP1A1 (− 6.7 kcal/mol) demonstrated the strongest binding affinities. MMP13 is overexpressed in lung adenocarcinoma, promoting tumor progression. Associated genes are enriched in extracellular matrix remodeling, inflammatory signaling, and the PI3K-Akt pathway. Conversely, CYP1A1 is downregulated and exhibits tumor-suppressive effects, with its interaction network enriched in cytochrome P450-mediated drug metabolism pathways.

Conclusion

1,4-DCB may participate in the pathogenesis of LUAD through multiple pathways by interacting with MMP13 and CYP1A1, providing scientific basis for risk assessment, diagnosis, and intervention in LUAD.

Graphical Abstract