双A在促进食道癌的分子机制基于网络毒理学和分子对接
Ming Hou1, Hanbing Jia2, Chongyang Liu1
1Department of Thoracic Surgery, The Second Hospital & Clinical Medical School, Lanzhou University, Lanzhou, China.
Medicine
|December 30, 2025
概括
双A (BPA) 是一种内分泌干扰物,可能通过影响HSP90AA1/HSP90AB1通路来促进食道癌 (ESCA). 这项研究揭示了ESCA预防和治疗的潜在分子标.
科学领域:
- 环境毒理学环境毒理学
- 分子瘤学分子瘤学
- 生物信息学是一种生物信息学.
背景情况:
- 双甲 (BPA) 是一种内分泌干扰化学物质,具有与各种癌症相关的雌激素活性.
- 通过BPA促进食道癌 (ESCA) 进展的特定分子机制尚不清楚.
研究的目的:
- 阐明BPA可能促进ESCA进展的分子途径.
- 根据BPA的行动,确定ESCA的潜在治疗目标.
主要方法:
- 网络毒理学方法集成多个公共数据库来识别BPA目标和ESCA相关基因.
- 蛋白质与蛋白质相互作用 (PPI) 网络分析,丰富分析和分子对接以确定关键基因和相互作用.
- 使用癌症基因图集 (TCGA) 进行基因表达,生存分析和cBioPortal进行突变分析的验证.
主要成果:
- 确定了BPA和ESCA之间95个重叠的目标,突出显示HSP90AA1和HSP90AB1作为中央枢纽基因.
- BPA对HSP90AA1和HSP90AB1.1表现出强烈的结合亲和力.
- 在ESCA组织中,HSP90AA1和HSP90AB1的高表达与生存率较差相关,HSP90AB1的变异频率很高.
结论:
- 乙A可能会通过通过HSP90AA1/HSP90AB1.1介导的瘤和免疫炎症途径推动ESCA的进展.
- 这些发现提高了对环境致癌性的理解,并建议HSP90AA1/HSP90AB1作为ESCA干预的潜在目标.
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