Pancreatic Cancer and Platelets Crosstalk: A Potential Biomarker and Target

Abstract

Platelets have been recognized as key players in hemostasis, thrombosis, and cancer. Preclinical and clinical researches evidenced that tumorigenesis and metastasis can be promoted by platelets through a wide variety of crosstalk between cancer cells and platelets. Pancreatic cancer is a devastating disease with high morbidity and mortality worldwide. Although the relationship between pancreatic cancer and platelets in clinical diagnosis is described, the interplay between pancreatic cancer and platelets, the underlying pathological mechanism and pathways remain a matter of intensive study. This review summaries recent researches in connections between platelets and pancreatic cancer. The existing data showed different underlying mechanisms were involved in their complex crosstalk. Typically, pancreatic tumor accelerates platelet aggregation which forms thrombosis. Furthermore, extracellular vesicles released by platelets promote communication in a neoplastic microenvironment and illustrate how these interactions drive disease progression. We also discuss the advantages of novel model organoids in pancreatic cancer research. A more in-depth understanding of tumor and platelets crosstalk which is based on organoids and translational therapies may provide potential diagnostic and therapeutic strategies for pancreatic cancer progression.

Keywords: TCIPA; angiogenesis; biomarker; organoids; pancreatic cancer; platelet extracellular vesicles; platelet-derived factors; platelets.

FIGURE 1

Schematic overview of crosstalk between platelets and pancreatic cancer. Pancreatic cancer can stimulate platelet activation and aggregation (TCIPA), change platelet shapes, and increase platelets’ release of microparticles with loading factors. However, platelet activation releases different kinds of factors, small molecules, and microparticles, which facilitate tumor growth, invasion, and metastasis. In the bloodstream, the tumor cell is surrounded by platelets that protect the encircled tumor cell from immune attack. In addition, platelets increase the properties of cancer cell adhesion and extravasation, thereby supporting cancer cell transmigration and metastasis. The intervention or inhibition of potential drugs in crosstalk between cancer and platelets are shown in the process.