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. 2017 Apr 12;18(4):809. doi: 10.3390/ijms18040809

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© 2017 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Potential coagulation factor-driven inflammatory responses within TME of EOC exposed to hypoxia. The coagulation factors derived from circulation, stromal cells, and cancer cells can connect EOC cells to platelets and leukocytes. Cell surface receptors and protease can also be activated under hypoxia, potentially transmitting cellular signaling. These molecular events are expected to facilitate survival and metastatic potential of EOC cells. Fb: fibroblast; CAF: cancer-associated fibroblast; TAM: tumor-associated macrophage; Mph: macrophage; Col: collagen; Hln: hyaluronan; PT: prothrombin: Fng; fibrinogen; VEGF: vascular endothelial growth factor; TIF: tissue interstitial fluid; EVs: extracellular vesicles; TNF-α: tumor necrosis factor-α. Dashed lines are indicative of non-covalent association. T-bars indicate suppression process. : secretion; : interaction; : intracellular signaling.

Inline graphic — Potential coagulation factor-driven inflammatory responses within TME of EOC exposed to hypoxia. The coagulation factors derived from circulation, stromal cells, and cancer cells can connect EOC cells to platelets and leukocytes. Cell surface receptors and protease can also be activated under hypoxia, potentially transmitting cellular signaling. These molecular events are expected to facilitate survival and metastatic potential of EOC cells. Fb: fibroblast; CAF: cancer-associated fibroblast; TAM: tumor-associated macrophage; Mph: macrophage; Col: collagen; Hln: hyaluronan; PT: prothrombin: Fng; fibrinogen; VEGF: vascular endothelial growth factor; TIF: tissue interstitial fluid; EVs: extracellular vesicles; TNF-α: tumor necrosis factor-α. Dashed lines are indicative of non-covalent association. T-bars indicate suppression process. : secretion; : interaction; : intracellular signaling.