Abstract
Tissue factor (TF) is a cell surface receptor for coagulation factor VII (fVII). The TF-activated fVII (fVIIa) complex is an essential initiator of the extrinsic blood coagulation process. Interactions between cancer cells and immune cells via coagulation factors and adhesion molecules can promote progression of cancer, including epithelial ovarian cancer (EOC). This process is not necessarily advantageous, as tumor tissues generally undergo hypoxia due to aberrant vasculature, followed by reduced access to plasma components such as coagulation factors. However, hypoxia can activate TF expression. Expression of fVII, intercellular adhesion molecule-1 (ICAM-1), and multiple pro-inflammatory cytokines can be synergistically induced in EOC cells in response to hypoxia along with serum deprivation. Thus, pro-inflammatory responses associated with the TF-fVIIa–ICAM-1 interaction are expected within hypoxic tissues. Tumor tissue consists of multiple components such as stromal cells, interstitial fluid, albumin, and other micro-factors such as proton and metal ions. These factors, together with metabolism reprogramming in response to hypoxia and followed by functional modification of TF, may contribute to coagulation factor-driven inflammatory responses in EOC tissues. The aim of this review was to describe potential coagulation factor-driven inflammatory responses in hypoxic EOC tissues. Arguments were extended to clinical issues targeting this characteristic tumor environment.
Highlights
Epithelial ovarian cancer (EOC) is a general term representing neoplasms in the pelvic or peritoneal cavity, as the origin of most EOC cases is not the ovary [1]
Cellular expression levels of proteins discussed in this review such as coagulation factors and intercellular adhesion molecule-1 (ICAM-1) would differ depending on cancer cell types and tumor components
It is possible that the Tissue factor (TF)-fVIIa complex triggers calcium (fVIIa) complex and ICAM-1 are significantly involved in this mechanism under these harsh conditions
Summary
Epithelial ovarian cancer (EOC) is a general term representing neoplasms in the pelvic or peritoneal cavity, as the origin of most EOC cases is not the ovary [1]. TF functions as a receptor for fVII, andX initiates the extrinsic blood coagulation cascade, including generation of activated factor. TF-fVIIa complex triggers a series of enzymatic reactions, leading to clot formation composed composed of platelets and red blood cells covered with fibrin polymers. The within the TF-fVIIa complex triggers a series of enzymatic reactions, leading to clot formation of platelets and red blood cells covered with fibrin polymers for. The gene encoding intercellular adhesion molecule-1 (ICAM-1), a cell surface mediator of the immune response, is robustly expressed in CCC cells in response to simultaneous exposure to hypoxia and serum deprivation conditions [34] This experimental evidence implies that inflammatory responses mediated via the cancer cell-derived TF-fVIIa complex and ICAM-1 play vital roles in EOC progression. Potential Relationship between Blood Coagulation and Inflammatory Factors in EOC Tissue: Overview of Current Knowledge
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