부산대학교 도서관

Simple Summary: Blood coagulation and cancer are intrinsically related; hyper-thrombotic complications are often observed in certain types of tumors. On the other hand, coagulation proteases are shown to promote the progression of cancer in a variety of unique mechanisms. The present review highlights how coagulation protease-induced signaling contributes to the immune evasion of different cancers, leading to the development and progression of cancer. Understanding the mechanistic insights will aid developing novel therapeutics against coagulation protease-driven response, which could be used in combination with conventional immune checkpoint inhibitors to increase the efficacy of cancer treatment and patient survival. Blood coagulation and cancer are intrinsically connected, hypercoagulation-associated thrombotic complications are commonly observed in certain types of cancer, often leading to decreased survival in cancer patients. Apart from the common role in coagulation, coagulation proteases often trigger intracellular signaling in various cancers via the activation of a G protein-coupled receptor superfamily protease: protease-activated receptors (PARs). Although the role of PARs is well-established in the development and progression of certain types of cancer, their impact on cancer immune response is only just emerging. The present review highlights how coagulation protease-driven PAR signaling plays a key role in modulating innate and adaptive immune responses. This is followed by a detailed discussion on the contribution of coagulation protease-induced signaling in cancer immune evasion, thereby supporting the growth and development of certain tumors. A special section of the review demonstrates the role of coagulation proteases, thrombin, factor VIIa, and factor Xa in cancer immune evasion. Targeting coagulation protease-induced signaling might be a potential therapeutic strategy to boost the immune surveillance mechanism of a host fighting against cancer, thereby augmenting the clinical consequences of targeted immunotherapeutic regimens. [ABSTRACT FROM AUTHOR]