Why the study?
Venous thromboembolism contributes to morbidity and mortality in women with ovarian cancer, but the underlying mechanisms of venous thrombosis are not well-understood.
Do tissue factor-bearing extracellular vesicles from ovarian cancer cells promote platelet aggregation and venous thrombosis in preclinical models?
Do tissue factor-bearing extracellular vesicles from ovarian cancer cells promote platelet aggregation and venous thrombosis in preclinical models?
Tissue factor-bearing extracellular vesicles from ovarian cancer cells promote platelet aggregation and venous thrombosis in preclinical models, suggesting a mechanism for cancer-associated VTE.
TF-EV effects on platelets may drive ovarian cancer VTE; hypothesis-generating, no clinical translation yet.
Venous thromboembolism (VTE) contributes to morbidity and mortality in women with ovarian cancer. Underlying mechanisms of venous thrombosis in ovarian cancer are not well-understood. The aim of this study was to identify the potential role of tissue factor (TF)-bearing extracellular vesicles (EVs) originated from cancer cells in venous thrombosis in ovarian cancer models. We examined the expression of TF on EVs generated by ovarian cancer cells and the effect of TF-positive EVs on platelet aggregation. Furthermore, we performed TF-knockdown or induced TF-overexpression in ovarian cancer cell lines and examined the effects of EVs obtained from these cells on platelet aggregation. We examined the effect of TF-bearing EVs originated from ovarian cancer cells on venous thrombosis in a mouse model of inferior vena cava (IVC) stenosis. TF was expressed in several ovarian cancer cell lines. EVs derived from ovarian cancer cell lines expressing TF promoted platelet aggregation. TF-knockdown in TF-high CAOV3 and OVCAR8 ovarian cancer cells delayed platelet aggregation induced by their EVs in vitro. Conversely, TF overexpression in TF-low A2780 and HeyA8 cells shortened platelet aggregation time induced by their EVs. EVs from TF-overexpressing A2780 cells enhanced thrombosis formation in the IVC stenosis model and resulted in a larger clot burden as compared to EVs from A2780 control cells. TF expression in ovarian cancer cell-derived EVs promoted platelet aggregation and thrombosis in preclinical models. These findings may have implications for reducing VTE rates in women with ovarian cancer.
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Sasano et al. (2020) studied this question.
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