Key result
EPCR and thrombomodulin co-expression drives protein C activation in cancer cells, blocked by anti-EPCR antibodies.
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Induction of procoagulant factors in malignant cells is considered to be the major cause of coagulation disorders in cancer. Thrombomodulin (TM), a negative regulator of coagulation was also found to be expressed in cancer cells. We report here evidence for another anticoagulant, the endothelial cell protein C receptor (EPCR), in cancer cells. EPCR was detected in several cell lines derived from various types of cancer. Significant levels of protein C (PC) activation were detected only with cell lines expressed both EPCR and TM. Anti-EPCR monoclonal antibodies (mAbs) specifically inhibited the activation. Thus, EPCR function appears to be important for PC activation by cancer cells. In addition, we detected EPCR expression in tumor cells from breast cancer patients, with an extremely high frequency. EPCR function may contribute to progression or pathogenesis of some types of cancer, and may explain the complexity of coagulopathy in cancer patients.
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Tsuneyoshi et al. (2001) studied Cancer (including breast cancer) and cancer-associated coagulopathy. Endothelial cell protein C receptor (EPCR) expression and anti-EPCR monoclonal antibodies was evaluated on Protein C (PC) activation and EPCR expression in cancer cells. Endothelial cell protein C receptor (EPCR) and thrombomodulin co-expression enabled significant protein C activation in cancer cell lines, which was inhibited by anti-EPCR monoclonal antibodies.
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