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Status |
Public on Jul 14, 2009 |
Title |
IKKα Is Required to Maintain Skin Homeostasis and Prevent Skin Cancer |
Organism |
Mus musculus |
Experiment type |
Expression profiling by array
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Summary |
It has long been known that excessive mitotic activity due to H-Ras can block keratinocyte differentiation and cause skin cancer. It is not clear, however, whether there are any innate surveillants that ensure keratinocytes undergoing terminal differentiation, preventing the disease. IKKα induces keratinocyte terminal differentiation and its reduction promotes skin tumor development. However, its nature function in skin cancer is unknown. Here we found that mice with IKKα deletion in keratinocytes or in hair follicle keratinocytes developed a thickened epidermis and spontaneous squamous cell-like carcinomas. Inactivation of epidermal growth factor receptor (EGFR) or reintroduction of IKKα inhibited excessive mitosis, induced terminal differentiation, and prevented skin cancer through an EGFR-driven autocrine loop in mice. Thus, IKKα serves as an innate surveillant.
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Overall design |
The differences in gene expression profiles of CHUK deleted mouse keratinocytes compared to wild type mouse keratinocytes were analyzed using two dual-channel agilent microarrays in duplicates.
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Contributor(s) |
Liu B, Xia X, Zhu F, Park E, Carbaj S, Kiguchi K, DiGiovanni J, Fischer S, Hu Y |
Citation missing |
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Submission date |
Jul 14, 2008 |
Last update date |
May 10, 2018 |
Contact name |
Yinling Hu |
E-mail(s) |
yhu@mdanderson.org
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Phone |
512-237 9338
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Fax |
512-237 2475
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Organization name |
UT M.D.Andreson Cancer Center
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Department |
Carcinogenesis
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Lab |
3
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Street address |
1808 Park Road 1C
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City |
Smithville |
State/province |
TX |
ZIP/Postal code |
78957 |
Country |
USA |
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Platforms (1) |
GPL4134 |
Agilent-014868 Whole Mouse Genome Microarray 4x44K G4122F (Feature Number version) |
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Samples (2) |
GSM305472 |
Wild Type Keratinocyte vs CHUK-LoxP Mutant Keratinocyte_rep1 |
GSM305473 |
Wild Type Keratinocyte vs CHUK-LoxP Mutant Keratinocyte_rep2 |
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Relations |
BioProject |
PRJNA113807 |