• Ovarian cancer;
  • Integrin αvβ5;
  • Vitronectin;
  • Adhesion;
  • Migration


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.