AP1 Transcription Factors in Epidermal Differentiation and Skin Cancer
Open Access
- 23 May 2013
- journal article
- review article
- Published by Hindawi Limited in Journal of Skin Cancer
- Vol. 2013, 1-9
- https://doi.org/10.1155/2013/537028
Abstract
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.This publication has 113 references indexed in Scilit:
- Protein Arginine Methyltransferase 5 (PRMT5) Signaling Suppresses Protein Kinase Cδ- and p38δ-dependent Signaling and Keratinocyte DifferentiationOnline Journal of Public Health Informatics, 2012
- c-Jun Promotes whereas JunB Inhibits Epidermal NeoplasiaJournal of Investigative Dermatology, 2011
- AP1 factor inactivation in the suprabasal epidermis causes increased epidermal hyperproliferation and hyperkeratosis but reduced carcinogen-dependent tumor formationOncogene, 2010
- Systemic anti-VEGF treatment strongly reduces skin inflammation in a mouse model of psoriasisProceedings of the National Academy of Sciences of the United States of America, 2009
- Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signalingProceedings of the National Academy of Sciences of the United States of America, 2009
- TNFα shedding and epidermal inflammation are controlled by Jun proteinsJournal of Bone and Joint Surgery, 2009
- Sulfiredoxin is an AP-1 target gene that is required for transformation and shows elevated expression in human skin malignanciesProceedings of the National Academy of Sciences of the United States of America, 2008
- Suppressor role of activating transcription factor 2 (ATF2) in skin cancerProceedings of the National Academy of Sciences of the United States of America, 2008
- Epithelial Stem Cells: Turning over New LeavesCell, 2007
- AP-1 in cell proliferation and survivalOncogene, 2001