{"title":"Platelet activation: a barrier to effective antitumor immunity","authors":"Daolin Tang, Rui Kang","doi":"10.1038/s41417-025-00915-7","DOIUrl":null,"url":null,"abstract":"Platelets, traditionally known for their role in hemostasis, are now recognized as key modulators of oncological processes, influencing tumor growth and metastasis through interactions with the tumor microenvironment. Recent studies reveal that platelet activation contributes to T-cell exhaustion by releasing thromboxane A2 (TXA2), which binds to the TBXA2R receptor and activates ARHGEF1, a guanine nucleotide exchange factor (GEF), leading to the suppression of T-cell function. This editorial explores the potential of repurposing anti-platelet drugs, such as aspirin, to counteract these effects. Aspirin, by inhibiting cyclooxygenase enzymes essential for TXA2 synthesis, can enhance T-cell activity in metastatic contexts, thereby improving immune surveillance and response. We advocate for further investigation into the thromboxane pathway’s impact on T-cell functionality and the development of aspirin-based therapeutic strategies to combat cancer metastasis.","PeriodicalId":9577,"journal":{"name":"Cancer gene therapy","volume":"32 7","pages":"741-743"},"PeriodicalIF":5.0000,"publicationDate":"2025-05-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.comhttps://www.nature.com/articles/s41417-025-00915-7.pdf","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer gene therapy","FirstCategoryId":"3","ListUrlMain":"https://www.nature.com/articles/s41417-025-00915-7","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOTECHNOLOGY & APPLIED MICROBIOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Platelets, traditionally known for their role in hemostasis, are now recognized as key modulators of oncological processes, influencing tumor growth and metastasis through interactions with the tumor microenvironment. Recent studies reveal that platelet activation contributes to T-cell exhaustion by releasing thromboxane A2 (TXA2), which binds to the TBXA2R receptor and activates ARHGEF1, a guanine nucleotide exchange factor (GEF), leading to the suppression of T-cell function. This editorial explores the potential of repurposing anti-platelet drugs, such as aspirin, to counteract these effects. Aspirin, by inhibiting cyclooxygenase enzymes essential for TXA2 synthesis, can enhance T-cell activity in metastatic contexts, thereby improving immune surveillance and response. We advocate for further investigation into the thromboxane pathway’s impact on T-cell functionality and the development of aspirin-based therapeutic strategies to combat cancer metastasis.
期刊介绍:
Cancer Gene Therapy is the essential gene and cellular therapy resource for cancer researchers and clinicians, keeping readers up to date with the latest developments in gene and cellular therapies for cancer. The journal publishes original laboratory and clinical research papers, case reports and review articles. Publication topics include RNAi approaches, drug resistance, hematopoietic progenitor cell gene transfer, cancer stem cells, cellular therapies, homologous recombination, ribozyme technology, antisense technology, tumor immunotherapy and tumor suppressors, translational research, cancer therapy, gene delivery systems (viral and non-viral), anti-gene therapy (antisense, siRNA & ribozymes), apoptosis; mechanisms and therapies, vaccine development, immunology and immunotherapy, DNA synthesis and repair.
Cancer Gene Therapy publishes the results of laboratory investigations, preclinical studies, and clinical trials in the field of gene transfer/gene therapy and cellular therapies as applied to cancer research. Types of articles published include original research articles; case reports; brief communications; review articles in the main fields of drug resistance/sensitivity, gene therapy, cellular therapy, tumor suppressor and anti-oncogene therapy, cytokine/tumor immunotherapy, etc.; industry perspectives; and letters to the editor.