Amir Hossein Kheirkhah, Tahereh Zarei Taher, Zahra Khosrowpour, Omid Mahmoudian, Maria Kavianpour
{"title":"The molecular mechanisms of platelets in tumor invasion and metastasis: a controversial role.","authors":"Amir Hossein Kheirkhah, Tahereh Zarei Taher, Zahra Khosrowpour, Omid Mahmoudian, Maria Kavianpour","doi":"10.1080/15384047.2026.2692154","DOIUrl":null,"url":null,"abstract":"<p><p>Platelets, traditionally recognized for their role in hemostasis, are now understood to actively contribute to tumor progression, angiogenesis, and metastasis. Through dynamic bidirectional interactions with cancer cells, platelets undergo measurable alterations in count, mean platelet volume, and molecular cargo, including proteins and mRNAs, supporting their potential utility as liquid biopsy biomarkers for early cancer detection. Within the tumor microenvironment, platelets contribute to immune evasion, support tumor cell intravasation and extravasation, enhance the survival of circulating tumor cells, and promote neovascularization. In addition, they can physically shield malignant cells from immune surveillance, thereby increasing metastatic potential. Although context-specific anti-tumor effects have been reported, the predominant evidence supports a largely pro-tumorigenic and pro-metastatic role for platelets. Elucidating the molecular mechanisms underlying platelet-tumor interactions is therefore essential for improving cancer risk stratification, prognostic evaluation, and therapeutic development. This review summarizes current advances in platelet-derived biomarkers and discusses emerging therapeutic strategies targeting platelet-mediated pathways to suppress metastasis and improve clinical outcomes in cancer patients.</p>","PeriodicalId":9536,"journal":{"name":"Cancer Biology & Therapy","volume":"27 1","pages":"2692154"},"PeriodicalIF":5.7000,"publicationDate":"2026-12-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13471101/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer Biology & Therapy","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1080/15384047.2026.2692154","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2026/8/11 0:00:00","PubModel":"Epub","JCR":"Q2","JCRName":"ONCOLOGY","Score":null,"Total":0}
引用次数: 0
Abstract
Platelets, traditionally recognized for their role in hemostasis, are now understood to actively contribute to tumor progression, angiogenesis, and metastasis. Through dynamic bidirectional interactions with cancer cells, platelets undergo measurable alterations in count, mean platelet volume, and molecular cargo, including proteins and mRNAs, supporting their potential utility as liquid biopsy biomarkers for early cancer detection. Within the tumor microenvironment, platelets contribute to immune evasion, support tumor cell intravasation and extravasation, enhance the survival of circulating tumor cells, and promote neovascularization. In addition, they can physically shield malignant cells from immune surveillance, thereby increasing metastatic potential. Although context-specific anti-tumor effects have been reported, the predominant evidence supports a largely pro-tumorigenic and pro-metastatic role for platelets. Elucidating the molecular mechanisms underlying platelet-tumor interactions is therefore essential for improving cancer risk stratification, prognostic evaluation, and therapeutic development. This review summarizes current advances in platelet-derived biomarkers and discusses emerging therapeutic strategies targeting platelet-mediated pathways to suppress metastasis and improve clinical outcomes in cancer patients.
期刊介绍：
Cancer, the second leading cause of death, is a heterogenous group of over 100 diseases. Cancer is characterized by disordered and deregulated cellular and stromal proliferation accompanied by reduced cell death with the ability to survive under stresses of nutrient and growth factor deprivation, hypoxia, and loss of cell-to-cell contacts. At the molecular level, cancer is a genetic disease that develops due to the accumulation of mutations over time in somatic cells. The phenotype includes genomic instability and chromosomal aneuploidy that allows for acceleration of genetic change. Malignant transformation and tumor progression of any cell requires immortalization, loss of checkpoint control, deregulation of growth, and survival. A tremendous amount has been learned about the numerous cellular and molecular genetic changes and the host-tumor interactions that accompany tumor development and progression. It is the goal of the field of Molecular Oncology to use this knowledge to understand cancer pathogenesis and drug action, as well as to develop more effective diagnostic and therapeutic strategies for cancer. This includes preventative strategies as well as approaches to treat metastases. With the availability of the human genome sequence and genomic and proteomic approaches, a wealth of tools and resources are generating even more information. The challenge will be to make biological sense out of the information, to develop appropriate models and hypotheses and to translate information for the clinicians and the benefit of their patients. Cancer Biology & Therapy aims to publish original research on the molecular basis of cancer, including articles with translational relevance to diagnosis or therapy. We will include timely reviews covering the broad scope of the journal. The journal will also publish op-ed pieces and meeting reports of interest. The goal is to foster communication and rapid exchange of information through timely publication of important results using traditional as well as electronic formats. The journal and the outstanding Editorial Board will strive to maintain the highest standards for excellence in all activities to generate a valuable resource.
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