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Molecular Cancer Research 5, 109-120, February 1, 2007. doi: 10.1158/1541-7786.MCR-06-0311
© 2007 American Association for Cancer Research

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Subject Review

The Activator Protein-1 Transcription Factor in Respiratory Epithelium Carcinogenesis

Michalis V. Karamouzis1, Panagiotis A. Konstantinopoulos1,2 and Athanasios G. Papavassiliou1

1 Department of Biological Chemistry, Medical School, University of Athens, Athens, Greece and 2 Division of Hematology-Oncology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, Massachusetts

Requests for reprints: Athanasios G. Papavassiliou, Department of Biological Chemistry, Medical School, University of Athens, 75 M. Asias Street, 11527 Athens, Greece. Phone: 30-210-7791207; Fax: 30-210-7791207. E-mail: papavas{at}med.uoa.gr

Abstract

Respiratory epithelium cancers are the leading cause of cancer-related death worldwide. The multistep natural history of carcinogenesis can be considered as a gradual accumulation of genetic and epigenetic aberrations, resulting in the deregulation of cellular homeostasis. Growing evidence suggests that cross-talk between membrane and nuclear receptor signaling pathways along with the activator protein-1 (AP-1) cascade and its cofactor network represent a pivotal molecular circuitry participating directly or indirectly in respiratory epithelium carcinogenesis. The crucial role of AP-1 transcription factor renders it an appealing target of future nuclear-directed anticancer therapeutic and chemoprevention approaches. In the present review, we will summarize the current knowledge regarding the implication of AP-1 proteins in respiratory epithelium carcinogenesis, highlight the ongoing research, and consider the future perspectives of their potential therapeutic interest. (Mol Cancer Res 2007;5(2):109–20)




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Copyright © 2007 by the American Association for Cancer Research.