Tissue factor (coagulation factor III): a potential double-edge molecule to be targeted and re-targeted toward cancer

A Integrins: The binding of TF-FVIIa to integrin leads turning to a high-affinity condition for these molecules. This complex formation is independent of TF-FVIIa potency for cleaving PAR. B Ephs: TF-FVIIa binary complex can cleave both Eph B 2/ A 2 proteolytically; then, signal transduction is induced by ephrins. C JAK-STAT Proteolytic activity of FVIIa causes initiating of apoptosis-related signaling events such as activation of PI3K, Akt, by STAT5 phosphorylation. D 1-Function of the MAP Kinase and PI3K-PKB pathways due to the TF-FVIIa interaction through activating specific transcription factors in the nucleus leads to the gene expression and translation of the synthesized m RNA. D 2-The signaling pathway is activated by a binary complex that consists SRC-like family, PI3K, PKB, and Rac stimulation conducts cytoskeletal rearrangement

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Tissue factor (coagulation factor III): a potential double-edge molecule to be targeted and re-targeted toward cancer. (2023) Seyed Esmaeil Ahmadi, et al. Biomark Res. 2023;11:60. Figure: F2. All organisms Drosophila melanogaster Homo sapiens

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