Authors

Luisa Pecorari, Department of Biomedical Sciences, Section of General Pathology, University of Modena and Reggio Emilia, 41100 Modena, ItalyFollow
Oriano Marin, CRIBI Biotechnology Center, Department of Biological Chemistry, University of Padova, 35122 Padova, ItalyFollow
Chiara Silvestri, Department of Biomedical Sciences, Section of General Pathology, University of Modena and Reggio Emilia, 41100 Modena, ItalyFollow
Olivia Candini, Department of Biomedical Sciences, Section of General Pathology, University of Modena and Reggio Emilia, 41100 Modena, ItalyFollow
Elena Rossi, Department of Biomedical Sciences, Section of General Pathology, University of Modena and Reggio Emilia, 41100 Modena, ItalyFollow
Clara Guerzoni, Department of Biomedical Sciences, Section of General Pathology, University of Modena and Reggio Emilia, 41100 Modena, ItalyFollow
Sara Cattelani, Department of Biomedical Sciences, Section of General Pathology, University of Modena and Reggio Emilia, 41100 Modena, ItalyFollow
Samanta A Mariani, Department of Biomedical Sciences, Section of General Pathology, University of Modena and Reggio Emilia, 41100 Modena, ItalyFollow
Francesca Corradini, Department of Biomedical Sciences, Section of General Pathology, University of Modena and Reggio Emilia, 41100 Modena, ItalyFollow
Giovanna Ferrari-Amorotti, Department of Biomedical Sciences, Section of General Pathology, University of Modena and Reggio Emilia, 41100 Modena, ItalyFollow
Laura Cortesi, Department of Oncology and Haematology, University of Modena and Reggio Emilia, 41100 Modena, ItalyFollow
Rita Bussolari, Department of Biomedical Sciences, Section of General Pathology, University of Modena and Reggio Emilia, 41100 Modena, ItalyFollow
Giuseppe Raschellà, ENEA Research Center Casaccia, Biotechnology Unit, Section of Toxicology and Biomedical Sciences, 00123 S. Maria di Galeria, Roma, ItalyFollow
Massimo R Federico, Department of Oncology and Haematology, University of Modena and Reggio Emilia, 41100 Modena, ItalyFollow
Bruno Calabretta, Department of Biomedical Sciences, Section of General Pathology, University of Modena and Reggio Emilia, 41100 Modena, Italy, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, 19197 USAFollow

Document Type

Article

Publication Date

1-1-2009

Comments

This article has been peer reviewed and is published in Molecular Cancer 2009, 8:58. The published version is available at DOI: 10.1186/1476-4598-8-58. Copyright © BioMed Central Ltd.

Abstract

BACKGROUND: Akt/PKB is a serine/threonine kinase that has attracted much attention because of its central role in regulating cell proliferation, survival, motility and angiogenesis. Activation of Akt in breast cancer portends aggressive tumour behaviour, resistance to hormone-, chemo-, and radiotherapy-induced apoptosis and it is correlated with decreased overall survival. Recent studies have identified novel tumor-specific substrates of Akt that may provide new diagnostic and prognostic markers and serve as therapeutic targets. This study was undertaken to identify pAkt-interacting proteins and to assess their biological roles in breast cancer cells. RESULTS: We confirmed that one of the pAkt interacting proteins is the Elongation Factor EF1alpha. EF1alpha contains a putative Akt phosphorylation site, but is not phosphorylated by pAkt1 or pAkt2, suggesting that it may function as a modulator of pAkt activity. Indeed, downregulation of EF1alpha expression by siRNAs led to markedly decreased expression of pAkt1 and to less extent of pAkt2 and was associated with reduced proliferation, survival and invasion of HCC1937 cells. Proliferation and survival was further reduced by combining EF1alpha siRNAs with specific pAkt inhibitors whereas EF1alpha downregulation slightly attenuated the decreased invasion induced by Akt inhibitors. CONCLUSION: We show here that EF1alpha is a pAkt-interacting protein which regulates pAkt levels. Since EF1alpha is often overexpressed in breast cancer, the consequences of EF1alpha increased levels for proliferation, survival and invasion will likely depend on the relative concentration of Akt1 and Akt2.

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