Platelet CLEC-2 and podoplanin in cancer metastasis.
It has long been recognised that the function of platelets in health and disease span far beyond their roles in haemostasis and thrombosis. The observation that tumour cells induce platelet aggregation was followed by extensive experimental evidence linking platelets to cancer progression. Aggregated platelets coat tumour cells during their transit through the bloodstream and mediate adherence to vascular endothelium, protection from shear stresses, evasion from immune molecules, and release of an array of bioactive molecules that facilitate tumour cell extravasation and growth at metastatic sites. The sialyated membrane glycoprotein podoplanin is found on the leading edge of tumour cells and is thought to influence their migratory and invasive properties. Podoplanin elicits powerful platelet aggregation and is the endogenous ligand for the platelet C-type lectin receptor, CLEC-2, which itself regulates podoplanin signalling. Here, the bidirectional relationship between CLEC-2 and podoplanin is described and considered in the context of tumour growth and metastasis.
Centre for Cardiovascular Sciences, Institute for Biomedical Research, College of Medical and Dental Sciences, University of Birmingham, Birmingham, B15 2TT, UK. kxl064@bham.ac.uk
Kate L
KL
Lowe
Leyre
L
Navarro-Nunez
Stephen P
SP
Watson
D000818:Animals; D001792:Blood Platelets / Q000378:metabolism*; D006801:Humans; D037181:Lectins, C-Type / Q000378:metabolism*; D008562:Membrane Glycoproteins / Q000378:metabolism*; D009362:Neoplasm Metastasis / Q000473:pathology / Q000503:physiopathology*; D000098853:Podoplanin
D037181:Lectins, C-Type; D008562:Membrane Glycoproteins; C104778:CLEC2B protein, human; C117468:PDPN protein, human; D000098853:Podoplanin