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Endothelial monocyte-activating polypeptide II (EMAP-II) is a tumor-derived cytokine that plays a critical role in inflammation, apoptosis, and angiogenesis within the tumor microenvironment.
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This review highlights the role of EMAP-II in modulating inflammation, apoptosis, and angiogenesis in the tumor microenvironment, which may inform future anti-cancer therapies.
The interactions between a tumor and its surrounding environment are complex and characterized by a variety of factors. Tumors produce a number of proteins that enable them to recruit a vascular supply, invade into surrounding tissues, and metastasize to distant sites. The host, in turn, responds to these signals by producing its own repertoire of molecules that may either assist or prevent the actions of the tumor. A thorough understanding of this relationship is critical to the development of novel anti-cancer therapies. The tumor-derived cytokine endothelial monocyte-activating polypeptide II (EMAP-II) has profound effects on the tumor as well as on host response. These effects target the inflammatory cascade as well as the processes involved in angiogenesis. In this review the authors describe the current understanding of the role of EMAP-II in inflammation, apoptosis, and angiogenesis and use this molecule to illustrate the complex interactions that occur in the tumor microenvironment.
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Berger et al. (2000) conducted a review in Cancer. Endothelial monocyte-activating polypeptide II (EMAP-II) was evaluated. Endothelial monocyte-activating polypeptide II (EMAP-II) is a tumor-derived cytokine that plays a critical role in inflammation, apoptosis, and angiogenesis within the tumor microenvironment.
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