通过网络毒理学和分子对接方法分析底层的分子机制di(2-ethylhexyl) phthalate诱导的膀癌症:一项观察性研究
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
概括
暴露于二甲基甲酸 (DEHP) 可能会因与关键蛋白和通路相互作用而导致膀癌 (BLCA). 本研究确定了涉及DEHP诱导BLCA发展的7个核心目标.
科学领域:
- 毒理学 毒理学 毒理学
- 分子生物学分子生物学
- 生物信息学是一种生物信息学.
背景情况:
- 2-乙烯基) 甲酸盐 (DEHP) 是一种常见的塑化剂,可疑具有致癌性.
- 了解DEHP诱导的膀癌 (BLCA) 的分子机制对于预防和治疗至关重要.
研究的目的:
- 调查DEHP的毒性,并阐明DEHP诱导的BLCA背后的分子机制.
- 通过网络毒理学和分子对接,确定涉及DEHP诱导BLCA的潜在分子标和途径.
主要方法:
- 网络毒理学的方法整合了多个数据库 (ChEMBL,STRING,GeneCards等). 为了确定DEHP的目标.
- 使用Cytoscape构建目标网络并分析核心目标.
- 基因本体学和KEGG通路丰富分析.
- 使用CB-Dock 2进行分子对接,以验证DEHP-目标相互作用.
主要成果:
- 确定了105个DEHP诱导BLCA的潜在目标,并选择了7个核心目标:CDK1,IL-6,CDK2,CCNB1,ERBB2,CCNB2和BCL2.
- 在瘤组织中观察到核心标的差异表达 (例如,IL-6和BCL2下调;CDK1,CDK2,CCNB1,ERBB2,CCNB2上调).
- 丰富分析显示,它参与了细胞信号传递和与癌症相关的途径. 分子对接证实了DEHP与核心目标的相互作用.
结论:
- DEHP可以通过与已识别的核心目标和相关信号通路的相互作用来促进BLCA的发展.
- 这项研究为了解DEHP诱导的BLCA提供了理论基础.
- 这些发现为未来的DEHP相关的膀癌的预防和治疗策略提供了潜在的参考.
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