http://www.cnr.it/ontology/cnr/individuo/prodotto/ID284091
Urokinase receptor promotes ovarian cancer cell dissemination through its 84-95 sequence (Articolo in rivista)
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- Urokinase receptor promotes ovarian cancer cell dissemination through its 84-95 sequence (Articolo in rivista) (literal)
- Anno
- 2014-01-01T00:00:00+01:00 (literal)
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Bifulco, Katia; Votta, Giuseppina; Ingangi, Vincenzo; Di Carluccio, Gioconda; Rea, Domenica; Losito, Simona; Montuori, Nunzia; Ragno, Pia; Stoppelli, Maria Patrizia; Arra, Claudio; Carriero, Maria Vincenza (2014)
Urokinase receptor promotes ovarian cancer cell dissemination through its 84-95 sequence
in Oncotarget
(literal)
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- Bifulco, Katia; Votta, Giuseppina; Ingangi, Vincenzo; Di Carluccio, Gioconda; Rea, Domenica; Losito, Simona; Montuori, Nunzia; Ragno, Pia; Stoppelli, Maria Patrizia; Arra, Claudio; Carriero, Maria Vincenza (literal)
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- Department of Experimental Oncology Unit, IRCCS Istituto Nazionale Tumori \"Fondazione G. Pascale\", Naples, Italy
Department of Experimental Pathology Unit, IRCCS Istituto Nazionale Tumori \"Fondazione G. Pascale\", Naples, Italy
Institute of Genetics and Biophysics \"Adriano Buzzati-Traverso\", National Research Council, Naples, Italy
Department of Translational Medical Sciences,\"Federico II\" University, Naples, Italy
Department of Chemistry and Biology, University of Salerno, Fisciano (Salerno), Italy (literal)
- Titolo
- Urokinase receptor promotes ovarian cancer cell dissemination through its 84-95 sequence (literal)
- Abstract
- The clinical relevance of the urokinase receptor (uPAR) as a prognostic marker in ovarian cancer is well documented. We had shown that the uPAR sequence corresponding to 84-95 residues, linking D1 and D2 domains (uPAR(84-95)), drives cell migration and angiogenesis in a protease-independent manner. This study was aimed at defining the contribution of uPAR(84-95) sequence to invasion of ovarian cancer cells. Now, we provide evidence that the ability of uPAR-expressing ovarian cancer cells to cross extra-cellular matrix and mesothelial monolayers is prevented by specific inhibitors of the uPAR(84-95) sequence. To specifically investigate uPAR(84-95) function, uPAR-negative CHO-K1 cells were stably transfected with cDNAs coding for uPAR D2 and D3 regions exposing (uPARD2D3) or lacking (uPAR Delta D2D3) the 84-95 sequence. CHO-K1/D2D3 cells were able to cross matrigel, mesothelial and endothelial monolayers more efficiently than CHO-K1/Delta D2D3 cells, which behave as CHO-K1 control cells. When orthotopically implanted in nude mice, tumor nodules generated by CHO-K1/D2D3 cells spreading to peritoneal cavity were more numerous as compared to CHO-K1/Delta D2D3 cells. Ovarian tumor size and intra-tumoral microvessel density were significantly reduced in the absence of uPAR(84-95). Our results indicate that cell associated uPAR promotes growth and abdominal dissemination of ovarian cancer cells mainly through its uPAR84-95 sequence. (literal)
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