Cell surface overexpression of αvβ5 integrin impedes αvβ3-mediated migration of the human ovarian adenocarcinoma cell line IGROV1

• Published in: Cell biology international Vol. 31; no. 2; pp. 109 - 118
• Main Authors: Maubant, Sylvie, Leroy-Dudal, Johanne, Carreiras, Franck, Deslandes, Edwige, Duigou, Françoise, Staedel, Cathy, Gauduchon, Pascal
• Format: Journal Article
• Language: English
• Published: Oxford, UK Elsevier Ltd 01.02.2007; Blackwell Publishing Ltd
• Subjects: Adhesion; Integrin αvβ5; Migration; Ovarian cancer; Vitronectin; Vitronectin; Integrin αvβ5; Adhesion; Migration; Ovarian cancer
• ISSN: 1065-6995; 1095-8355
• DOI: 10.1016/j.cellbi.2006.09.013

Human ovarian surface epithelium and epithelial tumors express integrin αvβ5, which can interact with vitronectin. In addition, in vitro acquisition of cisplatin resistance by αvβ3-expressing IGROV1 cells is accompanied by cell-surface expression of integrin αvβ5. To further explore the role of αvβ5 in ovarian carcinoma cells, IGROV1 cells were stably transfected with a human β5 integrin cDNA construct, and three β5 transfectant clones were selected for the expression of αvβ5 integrin at their cell surface. Despite a delayed entry in the exponential phase of growth, β5-transfectant cells kept a proliferation ability similar to that of parental cells, while their growth rate was hindered in the presence of an anti-αvβ5 blocking antibody. Only simultaneous blockade of αvβ3 and αvβ5 by specific antibodies impeded the adhesion to vitronectin of β5 transfectants and of the β5-expressing cisplatin-resistant variant IGROV1-R10, suggesting that the two heterodimers cooperated in the regulation of this process. Cell surface expression of αvβ5 resulted in an attenuation of αvβ3-mediated migration on vitronectin. αvβ5 participated to migration events in the absence of exogenous growth factors only in one transfectant clone and in IGROV1-R10 cells. Finally, the response to cisplatin was not significantly modified in β5 transfectants when compared to IGROV1 parental cells.