Scholarlink

Background <p>Benzo[a]pyrene (B[a]P), a ubiquitous environmental pollutant, is prevalent in emissions, food products, and tobacco. Although B[a]P’s carcinogenicity is well-established, the common molecular mechanisms underlying its pan-cancer carcinogenesis remain incompletely understood. This study systematically investigated B[a]P’s shared pathogenic mechanisms in 10 common solid tumors: bladder, breast, cervical, colorectal, esophageal, gastric, liver, lung, prostatic, and thyroid cancer.</p> Methods <p>Computational tools assessed B[a]P toxicity and identified targets. Disease targets for each cancer were retrieved from databases. Intersection analysis found candidate targets. Core targets were identified via protein-protein interaction network. GO/KEGG analyses revealed biological roles and pathways. The binding performance of B[a]P to the core targets was analyzed using molecular docking and molecular dynamics simulations.</p> Results <p>Cancer-specific potential toxicity targets were identified (range: <i>n</i> = 40–59). Enrichment analysis revealed conserved carcinogenic pathways across cancer types, including cellular response to xenobiotic stimuli, chemical carcinogen-induced receptor activation and DNA adduct formation, cytochrome P450-mediated xenobiotic metabolism, endocrine resistance, steroid hydroxylase activity, and calcium signaling pathways. Common core targets included ESR1, EGFR, MAPK3, MMP9, and PTGS2. Molecular docking and dynamics simulations confirmed strong B[a]P binding to these targets.</p> Conclusion <p>This study elucidated fundamental molecular features of B[a]P-induced pan-carcinogenesis, providing a theoretical framework for developing universal prevention and therapeutic strategies.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Integrated network toxicology, molecular docking, and molecular dynamics simulation reveals mechanisms of benzo[a]pyrene-induced pan-cancer

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年1月19日

查看全文
  • Yuxin Pan,
  • Shuqi Qin,
  • Cheng Chen,
  • Shaoyu He,
  • Manling Zhang,
  • Jiahao Hou,
  • Junzhi Wang,
  • Zhenting Wang,
  • Mingyi Zhao

摘要

Background

Benzo[a]pyrene (B[a]P), a ubiquitous environmental pollutant, is prevalent in emissions, food products, and tobacco. Although B[a]P’s carcinogenicity is well-established, the common molecular mechanisms underlying its pan-cancer carcinogenesis remain incompletely understood. This study systematically investigated B[a]P’s shared pathogenic mechanisms in 10 common solid tumors: bladder, breast, cervical, colorectal, esophageal, gastric, liver, lung, prostatic, and thyroid cancer.

Methods

Computational tools assessed B[a]P toxicity and identified targets. Disease targets for each cancer were retrieved from databases. Intersection analysis found candidate targets. Core targets were identified via protein-protein interaction network. GO/KEGG analyses revealed biological roles and pathways. The binding performance of B[a]P to the core targets was analyzed using molecular docking and molecular dynamics simulations.

Results

Cancer-specific potential toxicity targets were identified (range: n = 40–59). Enrichment analysis revealed conserved carcinogenic pathways across cancer types, including cellular response to xenobiotic stimuli, chemical carcinogen-induced receptor activation and DNA adduct formation, cytochrome P450-mediated xenobiotic metabolism, endocrine resistance, steroid hydroxylase activity, and calcium signaling pathways. Common core targets included ESR1, EGFR, MAPK3, MMP9, and PTGS2. Molecular docking and dynamics simulations confirmed strong B[a]P binding to these targets.

Conclusion

This study elucidated fundamental molecular features of B[a]P-induced pan-carcinogenesis, providing a theoretical framework for developing universal prevention and therapeutic strategies.