Altered adhesion properties and alphav integrin expression in a cisplatin-resistant human ovarian carcinoma cell line

In order to elucidate the mechanisms underlying the development of chemoresistance in ovarian cancer, we have previously established the IGROV1-R10 cisplatin-resistant cell line by mimicking a clinical protocol of drug administration on IGROV1 human ovarian carcinoma cells. Both IGROV1 and IGROV1-R1...

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Bibliographic Details
Published in:International journal of cancer 2002-01, Vol.97 (2), p.186-194
Main Authors: Maubant, Sylvie, Cruet-Hennequart, Séverine, Poulain, Laurent, Carreiras, Franck, Sichel, François, Luis, José, Staedel, Cathy, Gauduchon, Pascal
Format: Article
Language:English
Subjects:
Adenocarcinoma - drug therapy
Adenocarcinoma - metabolism
Adenocarcinoma - pathology
Antibodies, Monoclonal
Antineoplastic Agents - pharmacology
Bromodeoxyuridine - metabolism
Cell Adhesion
Cell Division - physiology
Cisplatin - pharmacology
DNA, Neoplasm - analysis
Drug Resistance, Neoplasm
Female
Flow Cytometry
Fluorescent Antibody Technique
Humans
Integrins - metabolism
Ovarian Neoplasms - drug therapy
Ovarian Neoplasms - metabolism
Ovarian Neoplasms - pathology
Receptors, Vitronectin - metabolism
Tumor Cells, Cultured - drug effects
Tumor Cells, Cultured - metabolism
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Summary:In order to elucidate the mechanisms underlying the development of chemoresistance in ovarian cancer, we have previously established the IGROV1-R10 cisplatin-resistant cell line by mimicking a clinical protocol of drug administration on IGROV1 human ovarian carcinoma cells. Both IGROV1 and IGROV1-R10 cells were able to grow as a monolayer and to release cell clusters into the medium. However, IGROV1-R10 cells exhibited an enhanced capacity to detach from the monolayer as compared to the parental cells. When substrate adhesion was prevented, IGROV1-R10 cells were able to survive and to proliferate as cell clusters, even at a low cell density, whereas IGROV1 cells massively died. To explore the underlying mechanisms, we have been interested in alphav integrins, which have been implicated in some aspects of ovarian cancer biology. Both IGROV1 and IGROV1-R10 adherent cells expressed alphavbeta3 integrin. During cell growth, alphavbeta5 integrin accumulated at the surface of a majority of IGROV1-R10 cells from the monolayer, whereas only a faint expression of this integrin was observed in a minority of IGROV1 cells. The growth of IGROV1-R10 cells, but not of IGROV1 cells, was partly inhibited by a specific alphavbeta5-blocking antibody suggesting that alphavbeta5 integrin contributed to IGROV1-R10 cell proliferation.
ISSN:0020-7136