Melanoma is the deadliest skin cancer whose rates have doubled over the last three decades, killing approximately 10,130 people annually. More than 90% of melanoma skin cancers develop because of cell damage from exposure to UV radiation, with UV exposure, frequent trips to the tanning salon and genetics all shown to play a role in developing skin cancer. Now, a study from researchers at the Keck School of Medicine of USC identifies a ‘sunscreen’ gene that is a tumour suppressor for skin cancer. The team state that if the global medical community understands how the ‘UV-resistant gene’ functions and the processes by which cells repair themselves after ultraviolet damage, then they could find targets for drugs to revert the misguided mechanism back to normal conditions. The opensource study is published in the journal Molecular Cell.
Previous studies show that the UV-resistant gene was identified nearly two decades ago in relation to a disease called Xeroderma Pigmentosum, which makes people extremely sensitive to sunlight and puts them at high risk for developing skin cancer. However, researchers did not examine the function of the UV-resistant gene in people who are healthy or who have skin cancer. The current study identified what the UV-resistant gene does and how it operates in a general population.
The current study used data from 340 melanoma patients who participated in The Cancer Genome Atlas, and included two experimental groups with either reduced levels of the UV-resistant gene or a mutant copy of that gene in melanoma cells and 50 fly eyes. The control groups were melanoma cells or fly eyes with normal copies of the UV-resistant gene. The lab gave a UV shot to cells carrying the normal UV-resistant gene and cells carrying defective copies of it. Results show that after 24 hours, cells carrying normal versions of the gene had repaired more than 50% of the UV-induced damage. Data findings show that, in contrast, the defective samples repaired less than 20% of the damaged cells.
The group explain that this suggests when people sunbathe or go tanning, those who have the normal UV-resistant gene can repair most UV-induced DNA burns in a timely manner, whereas those with the defective UV-resistant gene will have more damage left unrepaired. They go on to add that after daily accumulation, if the same people sunbathe or go tanning often, they will have increased risk for developing skin cancers such as melanoma. The researchers state that they were able to show a correlation with increased cancer risk, although the study did not definitively verify diminished levels or mutant copies of the UV-resistant gene were causes for skin cancer development.
Results show that the expression level of the UV-resistant gene is related to melanoma patients’ survival and metastasis stages. Data findings show that lower levels of the UV-resistant gene means a lower survival rate and advanced metastases stages. The lab note that, to their knowledge, the UV-resistant gene does not have any enzymatic activity, hypothesizing that primarily exists in a supporter or coordinator-role. They go on to add that although the gene may not be the direct doer, without it, the whole structure collapses and conclude that future studies in mouse models should provide better understanding as to how the UV-resistant gene functions.
The team surmise that their findings suggest the UV-resistant gene may serve as a biomarker for skin cancer prevention, and people who have the mutated UV-resistant gene or low levels of the UV-resistant gene may be at higher risk of melanoma or other skin cancers, especially if they go sunbathing or tanning frequently. For the future, the researchers state that it is hoped the drug may stimulate the reparable function of the UV-resistant gene to ensure swift and effective repair of UV-damaged skin cells.
Michelle is a health industry veteran who taught and worked in the field before training as a science journalist.
Featured by numerous prestigious brands and publishers, she specializes in clinical trial innovation--expertise she gained while working in multiple positions within the private sector, the NHS, and Oxford University.