Researchers have found that a gene which helps to control tumours also triggers the chemical chain reaction that makes the skin tan when exposed to ultraviolet (UV) light.
They believe the protein p53 also known as the “master watchman of the genome” for its ability to guard against cancer-causing DNA damage, prompts the skin to tan in response to ultraviolet light from the sun and deters the development of melanoma skin cancer, the fastest-increasing form of cancer in the world.
The team at the Dana-Farber Cancer Institute say the protein p53, is not only linked to skin tanning, but also may play a role in people’s love of being in the sun, an activity that, by promoting tanning, can reduce one’s risk of melanoma.
Dr. David E. Fisher, director of the Melanoma Program at Dana-Farber and a professor in pediatrics at the Children’s Hospital in Boston, says the number one risk factor for melanoma is an inability to tan and people who tan easily or have dark pigmentation are far less likely to develop the disease.
Dr. Fisher, the study’s senior author, says p53 which is one of the best-known tumour-suppressor proteins in the body, has a powerful role in protecting us against sun damage in the skin.
Fisher and his colleagues say the chain of events within keratinocytes that leads to alpha-MSH production, however was a mystery.
Even though they knew that alpha-MSH is created when another protein, known as pro-opiomelanocortin (or POMC), is split apart and that the amount of POMC within cells rises sharply when they’re exposed to UV rays, they didn’t know what caused the POMC to increase.
The researchers believed one possibility was p53 and when they examined the section of the gene for POMC that promotes production of the protein, they found it meshed neatly with p53 and increased the production of POMC.
This was supported by evidence following the exposure of human and mouse keratinocytes to UV radiation when after a six hour period, levels of both POMC and p53 were far higher than normal, and the level of pigment-stimulating alpha-MSH was 30 times above normal.
Further experiments confirmed this was the case but when they delivered UV radiation to mice whose keratinocytes lacked p53, POMC production was not induced and the mice did not tan.
The findings have implications beyond the issue of tanning, particularly in regard to hyperpigmentation, or age spots which appear in the elderly.
Fisher says the research offers a potential explanation of how this condition occurs, as p53 is a classic ‘stress’ protein and may trigger the hyperpigmentation process.
The researchers say there is even the possibility that p53 protects against skin damage in another way as the protein not only causes skin to tan in response to sunlight, it may also underlie people’s desire to spend time in the sun.
Fisher says the induction of beta-endorphin appears to be hard-wired to the tanning pathway, and might explain addictive behaviours associated with sun-seeking or the use of tanning salons.
The researchers say in future skin lotions may be able to activate p53 in just enough amounts to trigger tanning without allowing UV damage.
Fisher is apparently involved in a small biotechnology company working to develop such a product.
The study is published in the journal Cell.