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Journal of Skin Cancer
Volume 2013, Article ID 537028, 9 pages
Review Article

AP1 Transcription Factors in Epidermal Differentiation and Skin Cancer

1Department of Biochemistry and Molecular Biology, University of Maryland, School of Medicine, 108 North Greene Street, Rm 103, Baltimore, MD 21201, USA
2Department of Dermatology, University of Maryland, School of Medicine, Baltimore, MD 21201, USA
3Department of Obstetrics and Genecology and Reproductive Sciences, University of Maryland, School of Medicine, Baltimore, MD 21201, USA
4Department of Cell Biology, Cleveland Clinic Foundation, Cleveland, OH 44106, USA
5Department of Microbiology and Immunology, University of Maryland, School of Medicine, Baltimore, MD 21201, USA

Received 21 February 2013; Accepted 2 May 2013

Academic Editor: Deric L. Wheeler

Copyright © 2013 Richard L. Eckert et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


AP1 (jun/fos) transcription factors (c-jun, junB, junD, c-fos, FosB, Fra-1, and Fra-2) are key regulators of epidermal keratinocyte survival and differentiation and important drivers of cancer development. Understanding the role of these factors in epidermis is complicated by the fact that each protein is expressed, at different levels, in multiple cells layers in differentiating epidermis, and because AP1 transcription factors regulate competing processes (i.e., proliferation, apoptosis, and differentiation). Various in vivo genetic approaches have been used to study these proteins including targeted and conditional knockdown, overexpression, and expression of dominant-negative inactivating AP1 transcription factors in epidermis. Taken together, these studies suggest that individual AP1 transcription factors have different functions in the epidermis and in cancer development and that altering AP1 transcription factor function in the basal versus suprabasal layers differentially influences the epidermal differentiation response and disease and cancer development.