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Insulin-Like Growth Factor-II Bound to Vitronectin Enhances MCF-7 Breast Cancer Cell Migration

Tissue BioRegeneration and Integration Research Program, Center for Molecular Biotechnology, School of Life Sciences, Queensland University of Technology, Brisbane, Queensland 4000, Australia

Address all correspondence and requests for reprints to: Anthony M. Noble, Tissue BioRegeneration and Integration Program, Centre for Molecular Biotechnology, School of Life Sciences, Queensland University of Technology, GPO Box 2434, Brisbane, Queensland 4001, Australia. E-mail: a.noble{at}qut.edu.au.

We have previously reported that IGF-II binds the extracellular matrix protein vitronectin (VN) with an affinity similar to that for the type-1 IGF receptor (IGF-1R). In view of this finding, and given the cited role of VN in cell motility and adhesion, we aimed to elucidate the functional consequences of this interaction on cellular processes relevant to breast carcinoma. We demonstrate that this complex slightly inhibits cell attachment and has little effect on protein synthesis in MCF-7 breast cancer cells. However, prebinding IGF-II to immobilized VN was found to significantly enhance breast cancer cell migration through Transwells. Interestingly, IGF-II bound to VN, and not IGF-II in solution in the presence of VN, seems to be responsible for the effects on cell migration. Furthermore, studies using analogs of IGF-II with reduced affinity for the IGF-1R or IGF binding proteins indicate that this response involves the IGF-1R but is independent of IGF binding proteins. This is the first study demonstrating that IGF-II:VN complexes enhance migration of cells. This may prove to be especially relevant, given that overexpression of IGF-II and VN are features of many tumors.

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				B. G. Hollier, J. A. Kricker, D. R. Van Lonkhuyzen, D. I. Leavesley, and Z. Upton Substrate-Bound Insulin-Like Growth Factor (IGF)-I-IGF Binding Protein-Vitronectin-Stimulated Breast Cell Migration Is Enhanced by Coactivation of the Phosphatidylinositide 3-Kinase/AKT Pathway by {alpha}v-Integrins and the IGF-I Receptor Endocrinology, March 1, 2008; 149(3): 1075 - 1090. [Abstract] [Full Text] [PDF]