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Review
. 2023 Nov 1;24(21):15855.
doi: 10.3390/ijms242115855.

Bleeding and Thrombosis in Multiple Myeloma: Platelets as Key Players during Cell Interactions and Potential Use as Drug Delivery Systems

Anushka Kulkarni  1 , Despina Bazou  2 , Maria José Santos-Martinez  1   3   4
Affiliations
Review

Bleeding and Thrombosis in Multiple Myeloma: Platelets as Key Players during Cell Interactions and Potential Use as Drug Delivery Systems

Anushka Kulkarni et al. Int J Mol Sci. .

Abstract

Multiple myeloma (MM) is a hematological malignancy originated in the bone marrow and characterized by unhindered plasma cell proliferation that results in several clinical manifestations. Although the main role of blood platelets lies in hemostasis and thrombosis, platelets also play a pivotal role in a number of other pathological conditions. Platelets are the less-explored components from the tumor microenvironment in MM. Although some studies have recently revealed that MM cells have the ability to activate platelets even in the premalignant stage, this phenomenon has not been widely investigated in MM. Moreover, thrombocytopenia, along with bleeding, is commonly observed in those patients. In this review, we discuss the hemostatic disturbances observed in MM patients and the dynamic interaction between platelets and myeloma cells, along with present and future potential avenues for the use of platelets for diagnostic and therapeutic purposes.

Keywords: cancer; drug carrier; multiple myeloma; platelets.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Interaction between MM cells and platelets. MM cells express: CD38, S1P, PDGFR, PSGL-1, and Syndecan-1. CD38 could bind to CD31 expressed on resting platelets, whereas PSGL-1 could bind to P-selectin expressed on activated platelets. MM cells release IL-6 and several immunoglobulins, including IgG. IL-6 can indirectly increase platelet count by increasing thrombopoietin production. IgG binds low-affinity Fc receptor (FcR) for the constant region of IgG (FcγRIIa). During activation and subsequent aggregation, platelets release several factors including TGF-β1, PDGF, S1P, and VEGF. PDGF and S1P have affinity for PDGF and S1P receptors, respectively, resulting in angiogenesis and tumor proliferation. Syndecan-1 shed from MM cells can also bind to VEGF, promoting angiogenesis. PSGL-1: P-selectin glycoprotein ligand-1; ADP: adenosine diphosphate; IgG: immunoglobulin G; IL-6: interleukin-6; PAR: protease-activated receptor; TGF-β1: transforming growth factor β1; PDGF: platelet-derived growth factor; PDGFR: platelet-derived growth factor receptor.
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