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Review

Nucleotide Excision Repair and Vitamin D—Relevance for Skin Cancer Therapy

1
Department of Orthodontics, Medical University of Lodz, 92-216 Lodz, Poland
2
Department of Molecular Genetics, University of Lodz, 90-236 Lodz, Poland
*
Author to whom correspondence should be addressed.
Academic Editor: Roman Perez-Fernandez
Int. J. Mol. Sci. 2016, 17(4), 372; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms17040372
Received: 27 January 2016 / Revised: 2 March 2016 / Accepted: 4 March 2016 / Published: 6 April 2016
Ultraviolet (UV) radiation is involved in almost all skin cancer cases, but on the other hand, it stimulates the production of pre-vitamin D3, whose active metabolite, 1,25-dihydroxyvitamin D3 (1,25VD3), plays important physiological functions on binding with its receptor (vitamin D receptor, VDR). UV-induced DNA damages in the form of cyclobutane pyrimidine dimers or (6-4)-pyrimidine-pyrimidone photoproducts are frequently found in skin cancer and its precursors. Therefore, removing these lesions is essential for the prevention of skin cancer. As UV-induced DNA damages are repaired by nucleotide excision repair (NER), the interaction of 1,25VD3 with NER components can be important for skin cancer transformation. Several studies show that 1,25VD3 protects DNA against damage induced by UV, but the exact mechanism of this protection is not completely clear. 1,25VD3 was also shown to affect cell cycle regulation and apoptosis in several signaling pathways, so it can be considered as a potential modulator of the cellular DNA damage response, which is crucial for mutagenesis and cancer transformation. 1,25VD3 was shown to affect DNA repair and potentially NER through decreasing nitrosylation of DNA repair enzymes by NO overproduction by UV, but other mechanisms of the interaction between 1,25VD3 and NER machinery also are suggested. Therefore, the array of NER gene functioning could be analyzed and an appropriate amount of 1.25VD3 could be recommended to decrease UV-induced DNA damage important for skin cancer transformation. View Full-Text
Keywords: DNA damage; UV radiation; DNA repair; nucleotide excision repair; skin cancer; melanoma DNA damage; UV radiation; DNA repair; nucleotide excision repair; skin cancer; melanoma
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MDPI and ACS Style

Pawlowska, E.; Wysokinski, D.; Blasiak, J. Nucleotide Excision Repair and Vitamin D—Relevance for Skin Cancer Therapy. Int. J. Mol. Sci. 2016, 17, 372. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms17040372

AMA Style

Pawlowska E, Wysokinski D, Blasiak J. Nucleotide Excision Repair and Vitamin D—Relevance for Skin Cancer Therapy. International Journal of Molecular Sciences. 2016; 17(4):372. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms17040372

Chicago/Turabian Style

Pawlowska, Elzbieta, Daniel Wysokinski, and Janusz Blasiak. 2016. "Nucleotide Excision Repair and Vitamin D—Relevance for Skin Cancer Therapy" International Journal of Molecular Sciences 17, no. 4: 372. https://0-doi-org.brum.beds.ac.uk/10.3390/ijms17040372

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