Tumoral CD24 tunes platelet binding and pro-metastatic functions
Posted on: 16 June 2025 , updated on: 18 June 2025
Preprint posted on 15 April 2025
Categories: cancer biology
📖 Background 📖
Platelets, while best known for their roles in blood clotting, are increasingly appreciated as active players in cancer progression. In particular, platelets can bind to circulating tumour cells inside of blood vessels, which protects them from the immune system and enables their metastasis to distant organs. Despite evidence suggesting that platelet-associated tumour cells are more likely to complete their metastatic journey,1 the specific ligands and receptors connecting these two cells remain only partially understood. Uncovering how platelets bind to tumour cells and finding ways to prevent these attachments happening in circulation would therefore offer a novel approach to limit metastasis.
In their preprint, Mittelheisser and team identify CD24 on tumour cells as a key regulator for platelet binding and demonstrate its role in promoting lung metastasis in mouse models.
💡 Key Findings 💡
- CD24 allows tumour cells to ensnare activated platelets:
Taking inspiration from their previous work exploring platelets and metastatic outgrowth,2 the authors tested the platelet-binding properties of several mouse cancer cell lines and showed that the CD24high and highly metastatic triple negative breast cancer cell line 4T1 was able to bind more platelets than CD24low cells. Silencing CD24 expression with short hairpin RNA reversed the platelet binding properties of 4T1 cells, highlighting the importance of this specific receptor. - Loss of CD24 impairs metastasis in mice:
In mouse models of blood-borne metastasis, the authors demonstrated—using in vivo imaging over several time points—that lowering CD24 expression in breast cancer cells reduces their ability to colonise the lung.
Figure 1. The authors discover that platelets were much better at binding to tumour cells expressing high levels of CD24, a membrane-tethered glycoprotein receptor that can connect to cells via P-selectin (CD62p). Activated platelets express high levels of CD62p on their surface, suggesting that this is how they can preferentially bind to CD24-expressing tumour cells. Created using biorender.com.
🤔 Why I found this preprint interesting 🤔
I’ve studied platelet biology for over a decade, and I’m particularly interested in how platelets promote cancer progression. While animal models highlight the importance of platelets in metastasis, there is plenty more to learn about the underlying mechanisms and whether these can be targeted to improve the lives of cancer patients. In their preprint, the authors start by screening several cancer cells lines, comparing their known metastatic potential with their ability to bind platelets in vitro and their expression of platelet-binding receptors. I liked this unorthodox, yet refreshing approach, which led to their selection of CD24, which has been studied extensively as a cancer stem cell marker but not explored in the context of platelet biology. The authors show that CD24 can bind CD62p, which is highly expressed on the surface of activated platelets. Therefore, tumour cells expressing CD24 may hold a selective advantage when it comes to binding and retaining activated platelets to increase their chances of successful metastasis.
🎯 Takeaway message 🎯
Mittelheisser and colleagues provide compelling evidence that CD24 enhances tumour-platelet crosstalk, driving both the early intravascular seeding and prolonged outgrowth of tumour cells in the lung environment. This work expands our understanding of how cancer cells exploit platelets to their advantage and highlights CD24 as a possible therapeutic target in limiting platelet-tumour cell interactions and maybe even metastasis.
✅ References ✅
- Labelle M, Begum S, Hynes RO. Direct signaling between platelets and cancer cells induces an epithelial-mesenchymal-like transition and promotes metastasis. Cancer Cell. 2011;20:576-590. doi: 10.1016/j.ccr.2011.09.009
- Garcia-Leon MJ, Liboni C, Mittelheisser V, Bochler L, Follain G, Mouriaux C, Busnelli I, Larnicol A, Colin F, Peralta M, et al. Platelets favor the outgrowth of established metastases. Nat Commun. 2024;15:3297. doi: 10.1038/s41467-024-47516-w
doi: https://doi.org/10.1242/prelights.40868
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