Role of platelets and platelet receptors in cancer metastasis

Abstract

The interaction of tumor cells with platelets is a prerequisite for successful hematogenous metastatic dissemination. Upon tumor cell arrival in the blood, tumor cells immediately activate platelets to form a permissive microenvironment. Platelets protect tumor cells from shear forces and assault of NK cells, recruit myeloid cells by secretion of chemokines, and mediate an arrest of the tumor cell platelet embolus at the vascular wall. Subsequently, platelet-derived growth factors confer a mesenchymal-like phenotype to tumor cells and open the capillary endothelium to expedite extravasation in distant organs. Finally, platelet-secreted growth factors stimulate tumor cell proliferation to micrometastatic foci. This review provides a synopsis on the current literature on platelet-mediated effects in cancer metastasis and particularly focuses on platelet adhesion receptors and their role in metastasis. Immunoreceptor tyrosine-based activation motif (ITAM) and hemi ITAM (hemITAM) comprising receptors, especially, glycoprotein VI (GPVI), FcγRIIa, and C-type lectin-like-2 receptor (CLEC-2) are turned in the spotlight since several new mechanisms and contributions to metastasis have been attributed to this family of platelet receptors in the last years.

Prediction of severe illness due to COVID-19 based on an analysis of initial Fibrinogen to Albumin Ratio and Platelet count

“…Previous studies had uncovered that markedly elevated D-dimer levels were common in death patients with COVID-19 [8,9]. Similar to their results, we presumed that severe patients with COVID-19 had increased coagulation and fibrinolysis activity, marked by elevated D-dimer concentrations [10,11]. Notably, one severe patients in our study was developed into critical disease 7 day after admission with a D-dimer level of 13.61 mg/L, which further validated our speculation.…”

WITHDRAWN: Anti-Oncogenic Activities Exhibited By Secretomes Of Mesenchymal Stem Cells Are Mediated By Modulation Of KITLG and DKK1 Genes In Glioma Stem Cells.

“…We found that WJT spheres have up-regulated a coagulation cascade to recruit platelets as a survival strategy. Therefore suitable antithrombotic and antiplatelet concepts may be a valuable addition to future individualized, targeted therapies (76). However, the details of the molecular mechanism in platelet activation require further studies.…”

<p>Potential Diagnostic Value Of Combining Inflammatory Cell Ratios With Carcinoembryonic Antigen For Colorectal Cancer</p>

“…Platelets are conducive to tumor growth, angiogenesis and metastasis by producing growth and angiogenic factors, such as vascular endothelial growth factor and basic fibroblast growth factor. 27 Additionally, platelets provide favorable conditions for cancer cells by aggregating around them, including immune surveillance escape, shear stress protection, prosurvival signals, adhesion to the endothelium and extravasation. 28 Interactively, cancer cells, through their oncogenic transformation, can release many platelet agonists, such as adenosine diphosphate, thrombin, thromboxane and microparticles, which participate in platelet activation and contribute to thrombocythemia in cancer patients.…”