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释放的酸盐:通过多omics网络,单细胞洞察力和分子对接来解码卵巢癌发生

Junchan Yang¹, Min Luo¹, Hongjun Wang¹

¹Department of Gynecology, The Eighth Affiliated Hospital, Southern Medical University (The First People's Hospital of Shunde, Foshan), Foshan, 528308, Guangdong, China.

Journal of ovarian research

|June 14, 2025

概括

暴露于酸盐可能会通过改变细胞代谢和与SIRT1和PPARα等关键调节器相互作用来驱动卵巢癌. 这项研究确定了潜在的生物标志物和针对环境致癌物有针对性的干预措施的途径.

科学领域:

环境毒理学环境毒理学
分子瘤学分子瘤学
计算生物学是一种计算生物学.

背景情况:

流行病学研究表明,甲酸盐暴露与卵巢癌之间存在联系.
推动这种关联的精确分子机制仍然不清楚,阻碍了生物标志物的发现和预防.
这项研究旨在利用综合计算方法阐明甲酸盐驱动的致癌途径.

研究的目的:

系统地识别分子标和酸盐诱导的卵巢癌发生的途径.
为了弥合环境暴露和癌症发展之间的机制差距.
为制定有针对性的干预措施提供信息,并确定潜在的暴露生物标志物.

主要方法:

网络毒理学网络毒理学
多基因分析 (包括基因表达和单细胞数据)
分子对接模拟分子对接模拟

主要成果:

确定了234个潜在的甲酸目标,富含HIF-1信号和促进癌症的代谢途径.
确定了七个核心基因,其中六个 (GAPDH,CASP3,PPARG,ESR1,CYCS,SIRT1,CCND1) 在卵巢癌 (TCGA队列) 中差异表达.
分子对接证实了酸盐和六个核心蛋白质之间的特定结合相互作用,表明直接的分子干扰.

结论:

酸盐可能通过代谢重编程 (HIF-1α/糖解) 促进卵巢癌,与SIRT1/PPARα结合,并重塑瘤微环境.
调查结果为优先考虑环境致癌物和识别暴露生物标志物建立了一个框架.
强调SIRT1-HIF1-PPARα轴在与甲酸相关的卵巢癌病原发生的重要性,并建议重新评估甲酸的安全性.

关键词:

分子对接是分子对接.网络毒理学网络毒理学卵巢癌是发生在卵巢中的癌症.甲酸的含量甲酸的含量在ScCancerExplorer中使用.

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