Pandey Manoj, Rajput Monika, Singh Pooja, Shukla Mridula, Zhu Bin, Koshiol Jill
Department of Surgical Oncology, Institute of Medical Sciences, Banaras Hindu University, Varanasi 221005, India.
RRL, Dr. Lalpath Labs Ltd., Shivpur, Varanasi 221003, India.
Cancers (Basel). 2024 Jan 3;16(1):223. doi: 10.3390/cancers16010223.
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 ( and ), 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 of with , , , interleukin//, , , and pathways was identified. The results of the present study demonstrate that aspirin improves cancer survival by the interplay of 41 genes through a complex mechanism. is 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.
阿司匹林对癌症生存的益处存在争议。随机临床试验和队列研究的数据不一致，尽管一项荟萃分析表明，在标准治疗中添加阿司匹林时具有明显的生存优势。然而，阿司匹林改善癌症生存的机制尚不清楚。通过PubMed检索以识别报告与阿司匹林和癌症生存相关的基因和通路的文章。使用基于网络的工具进行基因本体和通路富集分析。评估基因-基因和蛋白质-蛋白质相互作用。识别并绘制通路之间的串扰。鉴定出41个基因，并将其分为主要基因（和）、调节细胞增殖的基因、白细胞介素和细胞因子基因以及DNA修复基因。网络分析显示这些基因和蛋白质之间存在丰富的基因-基因和蛋白质-蛋白质相互作用。通路富集显示，除了DNA修复、自噬、细胞外基质和凋亡通路外，白细胞介素和细胞转导通路是参与阿司匹林相关生存的主要通路。鉴定出与、、、白细胞介素//、、和通路的串扰。本研究结果表明，阿司匹林通过41个基因的相互作用，通过复杂机制改善癌症生存。是阿司匹林的主要靶点，并通过六个主要通路影响癌症生存：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。
