Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
5649421 | Journal of Investigative Dermatology | 2017 | 34 Pages |
Abstract
The nicotinamide adenine dinucleotide phosphate oxidase (NOX) family enzymes are involved in several physiological functions. However, their roles in keratinocyte responses to UV radiation have not been clearly elucidated. This study shows that, among other NOX family members, UVB irradiation results in a biphasic activation of NOX1 that plays a critical role in defining keratinocyte fate through the modulation of the DNA damage response network. Indeed, suppression of both bursts of UVB-induced NOX1 activation by using a specific peptide inhibitor of NOX1 (InhNOX1) is associated with increased nucleotide excision repair efficiency and reduction of apoptosis, which is finally translated into decreased photocarcinogenesis. On the contrary, when only the second peak of UVB-induced NOX1 activation is blocked, both nucleotide excision repair efficiency and apoptosis are decreased. Our results show that inhibition of NOX1 activation could be a promising target for the prevention and treatment of UVB-induced skin cancer in nucleotide excision repair-proficient and -deficient patients.
Keywords
Related Topics
Health Sciences
Medicine and Dentistry
Dermatology
Authors
Houssam Raad, Martin Serrano-Sanchez, Ghida Harfouche, Walid Mahfouf, Doriane Bortolotto, Vanessa Bergeron, Zeinab Kasraian, Lea Dousset, Mohsen Hosseini, Alain Taieb, Hamid Reza Rezvani,