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Fig. 8 | Journal of Experimental & Clinical Cancer Research

Fig. 8

From: Targeting the Formyl Peptide Receptor type 1 to prevent the adhesion of ovarian cancer cells onto mesothelium and subsequent invasion

Fig. 8

Schematic diagram of proposed mechanism of RI-3 inhibitory effects on EOC cell adhesion. After detachment from the primary tumor, EOC cells float in the peritoneal fluid. EOC cells able to adhere to mesothelial ECM components via integrins may penetrate mesothelial cell layers. Intact uPAR or uPAR-derived fragments containing the 84–95 sequence that are expressed on EOC cell surface or may be released in the ascitic fluid, bind to FPR1 generating a cascade of events. Once engaged, FPR1 internalizes, triggering αvβ3 vitronectin receptor activation which, in turn, allows EOC cells to adhere onto mesothelial Vn. Subsequently, proteases within the mesothelial milieu allow EOC cells to invade the mesothelial cell layer where they proliferate and form metastases. This process may be counteracted by nanomolar concentrations of RI-3 peptide, blocking the assembly of uPAR/FPR1 complexes

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