Researchers Link DNA Repair Protein With Increased Skin Cancer

Posted: October 31, 2011

Researchers from the University of North Carolina at Chapel Hill have established a connection between a repairing protein and times of the day with an increased risk of skin cancer.

In "Control of skin cancer by the circadian rhythm," an article appearing in the Proceedings of the National Academy of Sciences, Aziz Sancar and his colleagues suggest that avoiding UV radiation at certain times of the day when xeroderma pigmentosum group A (XPA) is low could lower skin cancer risk.

The team previously reported that the protein XPA, which is responsible for repairing the DNA damage caused by UV radiation, fluctuates throughout the day. According to the researchers, UV damage is removed by the nucleotide excision repair system in humans and mice, of which the XPA protein is a rate-limiting sub-unit.

The researchers exposed two groups of mice to UV radiation—either at 4 AM or at 4 PM—and waited for cancer to develop. Mice irradiated when the repair activity was at its minimum (4 AM) developed tumors much faster and 500% higher compared with mice exposed to UV when the protein's repair function was at its maximum (4 PM). They concluded that time of day of exposure to UVR is a contributing factor to its carcinogenicity in mice, and possibly in humans.

The researchers predict that humans will have a higher rate of DNA repair in the morning and would be less prone to the carcinogenic effect of UV radiation in the morning hours. Although mice and humans both reside on a 24-hour day, the "circadian" clocks of these nocturnal and diurnal creatures run counter each other. This key difference in biology means that humans are most protected from the sun's harmful rays when mice are most susceptible, and vice versa.