文章：

阿司匹林与癌症生存率：分子机制分析

Aspirin and Cancer Survival: An Analysis of Molecular Mechanisms

原文发布日期：3 January 2024

DOI: 10.3390/cancers16010223

类型: Article

开放获取: 是

英文摘要：

The benefit of aspirin on cancer survival is debated. Data from randomized clinical trials and cohort studies are discordant, although a meta-analysis shows a clear survival advantage when aspirin is added to the standard of care. However, the mechanism by which aspirin improves cancer survival is not clear. A PubMed search was carried out to identify articles reporting genes and pathways that are associated with aspirin and cancer survival. Gene ontology and pathway enrichment analysis was carried out using web-based tools. Gene–gene and protein–protein interactions were evaluated. Crosstalk between pathways was identified and plotted. Forty-one genes were identified and classified into primary genes (PTGS2andPTGES2), genes regulating cellular proliferation, interleukin and cytokine genes, and DNA repair genes. The network analysis showed a rich gene–gene and protein–protein interaction between these genes and proteins. Pathway enrichment showed the interleukin and cellular transduction pathways as the main pathways involved in aspirin-related survival, in addition to DNA repair, autophagy, extracellular matrix, and apoptosis pathways. Crosstalk ofPTGS2withEGFR,JAK/AKT,TP53, interleukin/TNFα/NFκB,GSK3B/BRCA/PARP,CXCR/MUC1, andWNT/CTNNBpathways was identified. The results of the present study demonstrate that aspirin improves cancer survival by the interplay of 41 genes through a complex mechanism.PTGS2is the primary target of aspirin and impacts cancer survival through six primary pathways: the interleukin pathway, extracellular matrix pathway, signal transduction pathway, apoptosis pathway, autophagy pathway, and DNA repair pathway.

摘要翻译： 

阿司匹林对癌症生存的获益尚存争议。尽管一项荟萃分析显示，在标准治疗基础上加用阿司匹林可带来明确的生存优势，但随机临床试验与队列研究的数据并不一致。然而，阿司匹林改善癌症生存的机制尚未明确。本研究通过PubMed检索，筛选出报道阿司匹林与癌症生存相关基因及通路的文献。利用网络工具进行基因本体论和通路富集分析，评估基因-基因及蛋白质-蛋白质相互作用，识别并绘制通路间的交互作用。共鉴定出41个基因，并将其分为核心基因（PTGS2与PTGES2）、细胞增殖调控基因、白细胞介素与细胞因子基因以及DNA修复基因。网络分析显示这些基因与蛋白质之间存在丰富的相互作用。通路富集分析表明，除DNA修复、自噬、细胞外基质和凋亡通路外，白细胞介素通路与细胞信号转导通路是阿司匹林相关生存的主要参与通路。研究发现PTGS2与EGFR、JAK/AKT、TP53、白细胞介素/TNFα/NFκB、GSK3B/BRCA/PARP、CXCR/MUC1及WNT/CTNNB通路存在交互作用。本研究结果表明，阿司匹林通过41个基因的复杂相互作用机制改善癌症生存。PTGS2是阿司匹林的主要作用靶点，通过六条核心通路影响癌症生存：白细胞介素通路、细胞外基质通路、信号转导通路、凋亡通路、自噬通路和DNA修复通路。

原文链接：

Aspirin and Cancer Survival: An Analysis of Molecular Mechanisms