by Alice Ren
It has become common knowledge that excessive exposure of the skin to UV rays (either in tanning beds or from sunlight) can cause skin cancer. First, let’s just outline what is meant by “skin cancer”: the 3 most common types are basal cell carcinoma (BCC), squamous cell carcinoma (SCC) and cutaneous malignant melanoma. These cancers all involve the abnormal growth of skin cells, often physically manifesting in the form of nodules, bumps and lesions within the tissue. The development of skin cancer is caused by exposure to UV rays, which is the only component of sunlight that is able to damage the DNA within skin cells by causing an accumulation of mutations eventually leading to cells becoming cancerous (ie carcinogenesis). In recent years, the concern for skin cancer has grown significantly due to the increase in human activities that deplete the ozone layer, such as the use of chlorofluorocarbons, which increases the risk as the protective layer of the earth has become thinner, leaving the skin exposed to the UV rays.
So how exactly do the skin cells become cancerous? The UV radiation damages the ability of cells to control proliferation (although cells have mechanisms in place to counteract this damage, such as DNA repair, apoptosis and immune surveillance). It also causes dimers to form in DNA between adjacent pyrimidine residues (the sugar parts of the nucleotide), which could potentially lead to UV-induced mutations that will accumulate over time. To repair this damage, the cells involved have 2 choices: repair the cell, or carry out apoptosis. If neither route is completed successfully, cell proliferation can spiral out of control, eventually causing a tumour to form via the inactivation of tumour suppressor genes, or the activation of oncogenes (genes that have the potential to cause cancer).
The mechanism by which UV radiation causes DNA damage and mutations begins with dimerised photoproducts, as mentioned above. There are 2 types of dimers formed: cyclobutane dimers between C4 and C5 carbons, between thymine or cytosine residues, and pyrimidine pyrimidone dimers (6-4) between any two adjacent pyrimidine residues. The
So how exactly do the skin cells become cancerous? The UV radiation damages the ability of cells to control proliferation (although cells have mechanisms in place to counteract this damage, such as DNA repair, apoptosis and immune surveillance). It also causes dimers to form in DNA between adjacent pyrimidine residues (the sugar parts of the nucleotide), which could potentially lead to UV-induced mutations that will accumulate over time. To repair this damage, the cells involved have 2 choices: repair the cell, or carry out apoptosis. If neither route is completed successfully, cell proliferation can spiral out of control, eventually causing a tumour to form via the inactivation of tumour suppressor genes, or the activation of oncogenes (genes that have the potential to cause cancer).
The mechanism by which UV radiation causes DNA damage and mutations begins with dimerised photoproducts, as mentioned above. There are 2 types of dimers formed: cyclobutane dimers between C4 and C5 carbons, between thymine or cytosine residues, and pyrimidine pyrimidone dimers (6-4) between any two adjacent pyrimidine residues. The cyclobutane dimers are around 3 times more common than the 6-4 photoproducts, however, both lesions occur the most frequently in “hotspot” areas of UV-induced damage, which are runs of tandem / repeated pyrimidine residues. The cyclobutane dimer is also the most mutagenic of the two, and is the major contributor to mutations in mammals (due to the 6-4 damage being repaired more rapidly by cells).
This then leads to questions about sunburn, and the well-known fact that getting sunburnt just once every 2 years can triple the risk of the development of skin cancer. Sunburn is a type of burn caused by UV radiation, and the redness that accompanies it is the inflammatory response of the skin tissue to the direct DNA damage caused by the UV rays. The lesions mentioned in the previous section can cause permanent mutations in skin DNA if not repaired, which leads to a large accumulation of many mutations. These include base insertions and deletions, which can dramatically change the base sequence and genes encoded, meaning that the genes that should usually control cellular processes such as proliferation, no longer have this control.
To prevent excessive UV-induced skin damage, regular sunscreen application is essential. Although it may seem futile to apply sunscreen in weather with high levels of cloud cover, UVA rays are able to penetrate through clouds, into the dermis (a deeper layer of the skin tissue), which can stimulate the production of oxygen free radicals in the skin. This then induces an oxidative stress, which can lead to indirect DNA damage where the free radicals modify DNA over a period of time. UVB rays, on the other hand, are significantly higher energy than UVA rays, but they do not penetrate the skin tissue as deeply. These rays are the primary cause of sunburn, and can be directly absorbed by the DNA of skin cells, potentially leading to the formation of a tumour due to lack of control over vital tumour suppressant cellular functions. UVB rays also play the most significant role in causing malignant melanoma, which is the most dangerous of the 3 common skin cancer types. Now we will see how sunscreen can prevent much of the damage caused by the different types of UV radiation. Physical sunscreens containing minerals like titanium dioxide or zinc oxide ground into fine powder are able to remain on top of the stratum corneum / skin surface, and reflect the UV rays away from the skin, thus preventing any penetration. Chemical sunscreens (or organic sunscreens) form a thin film on top of the skin surface, acting as a protective layer that can absorb UV rays before they penetrate the skin tissue. By implementing daily sunscreen use, especially when the sunlight is particularly powerful, the accumulation of DNA damage / mutations can be drastically reduced, hence also reducing the risk of skin cancer.
Hopefully you can see that UV exposure causes a lot more damage than most realise. The DNA damage becomes increasingly difficult to reverse / reduce as more mutations accumulate, so it would be wise to begin daily sunscreen use as early in life as possible in order to eliminate the chances of skin cancer developing. Not only will this help you avoid cancer, but it also hugely decreases the extent of photoageing and cosmetic damage to the skin (often leading to depletion of the extracellular matrix and increase in hyperpigmentation), which is also caused by UV rays.
Sources:
http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.534.788&rep=rep1&type=pdf
https://www.skincancer.org/skin-cancer-prevention/sun-protection/sunscreen/
https://www.sciencedirect.com/science/article/pii/S1011134401001981
https://www.livescience.com/38039-what-causes-sunburns.html
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