Platelet Dynamics in Cancer Progression

Platelets, traditionally recognised for their role in haemostasis, have emerged as pivotal mediators of cancer progression. Beyond clot formation, they interact dynamically with circulating tumour cells (CTCs), providing mechanical protection against shear stress and immune attack. Upon activation by tumour-derived signals, platelets release an array of growth factors, chemokines and microparticles that foster angiogenesis, stromal remodelling and epithelial–mesenchymal transition. These secreted mediators increase vascular permeability, enabling extravasation of tumour cells and seeding of distant organs. Moreover, platelets can infiltrate primary tumours, where they support local proliferation and modulate the immune microenvironment. Clinically, thrombocytosis often correlates with poor prognosis across multiple malignancies, and antiplatelet strategies are under investigation to hinder metastatic dissemination.

Research from Nature Portfolio

Recent studies have illuminated a precise molecular axis by which platelets confer survival advantages on detached cancer cells. In vitro experiments demonstrated that direct platelet contact activates a RhoA–MYPT1–PP1 cascade in tumour cells, resulting in dephosphorylation and nuclear translocation of the transcriptional coactivator YAP1. Once in the nucleus, YAP1 drives a pro-survival gene expression programme that prevents anoikis. In vivo models of induced thrombocytosis confirmed that platelet-mediated activation of YAP1 is critical for metastatic colonisation. Genetic knockdown or pharmacological inhibition of components of this pathway significantly reduced secondary tumour burden, highlighting a potential target to disrupt platelet-driven metastasis.

Platelet Dynamics in Cancer Progression publication trend

The graph below shows the total number of articles in platelet dynamics in cancer progression across all publications each year (not limited to Nature Index journals).

Technical terms

Anoikis: Programmed cell death triggered when cells detach from the surrounding extracellular matrix.

Circulating tumour cells (CTCs): Cancer cells that have shed into the bloodstream from primary or metastatic lesions.

Extravasation: The process by which cells migrate from the vascular compartment into surrounding tissues.

Tumour-educated platelets (TEPs): Platelets that acquire altered RNA profiles and phenotypes upon interaction with tumour-derived factors.

YAP1: A transcriptional coactivator regulated by phosphorylation, involved in cell survival and proliferation.

Glycoprotein VI (GPVI): A collagen receptor on platelets that mediates adhesion and activation.

C-type lectin-like receptor 2 (CLEC-2): A platelet activation receptor that binds podoplanin on tumour cells, promoting aggregation.

References

1. Role of platelets and platelet receptors in cancer metastasis. Journal of Hematology & Oncology (2018).
2. RNA-Seq of Tumor-Educated Platelets Enables Blood-Based Pan-Cancer, Multiclass, and Molecular Pathway Cancer Diagnostics. Cancer Cell (2015).
3. Swarm Intelligence-Enhanced Detection of Non-Small-Cell Lung Cancer Using Tumor-Educated Platelets. Cancer Cell (2017).
4. Platelets reduce anoikis and promote metastasis by activating YAP1 signaling. Nature Communications (2017).