环境中的暴露通过DHX34促进肺癌:一个分子毒理学观点
Yongbin Lu1, Weize Kong1, Kaiwen Wang2
1Evidence-Based Medicine Center, School of Basic Medical Sciences, Lanzhou University, Lanzhou, Gansu, China; Evidence-Based Social Science Research Center, Health Technology Assessment Center, School of Public Health, Lanzhou University, Lanzhou, Gansu, China; Gansu Key Laboratory of Evidence-Based Medicine, Lanzhou, Gansu, China.
Ecotoxicology and environmental safety
|September 20, 2025
概括
长期暴露于会增加癌症和肺癌死亡风险. 该研究确定DHX34是调解诱导肺癌进展的关键基因,提供潜在的治疗标.
科学领域:
- 环境健康 环境健康
- 分子生物学分子生物学
- 在瘤学瘤学.
背景情况:
- (Cd) 暴露与肺癌有关,但其对癌症死亡率和潜在分子机制的影响需要进一步调查.
- 目前关于Cd暴露和癌症死亡率的研究有限,需要进行全面评估.
研究的目的:
- 量化评估Cd暴露与癌症/肺癌死亡率之间的关联.
- 为了识别和验证参与Cd诱导肺癌发生的关键基因.
- 为了阐明Cd相关的肺癌进展的分子机制.
主要方法:
- 对Cd暴露和死亡率的队列研究的元分析.
- 生物信息学分析 (GSE165549,TCGA) 和LASSO回归.
- 门德尔的随机化,分子对接,分子动力学模拟,体外和体内测试.
主要成果:
- 长期Cd暴露显著增加了癌症死亡风险 (RR=1.49) 和肺癌死亡风险 (RR=1.86),特别是在男性中.
- 在细胞周期和DNA复制等途径中确定了36个Cd相关基因;DHX34被突出显示为与肺癌有因果关系.
- 暴露于Cd上调了DHX34,促进了肺癌细胞的增殖和瘤的生长,并证实了强大的Cd-DHX34结合 afinity.
结论:
- 在调解Cd诱导的肺癌进展方面,DHX34起着至关重要的作用.
- 环境中的重金属暴露,如,具有显著的致癌风险.
- 这些发现为Cd相关的肺癌的早期预防和治疗干预提供了潜在的分子标.
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