Epigenetics and Skin Cancer Prevention
In our previous blog posts we discussed the role played by UVB in initiating the development of skin cancer via direct DNA damage and production of free radicals. The good news on that front is that new research revealing the power of topical antioxidants and anti-inflammatories will eventually result in a new generation of safer and more effective sunscreens.
In the meantime, research in another field—epigenetics—is poised to change the way we look not just at sun protection, but skin care overall. Its impact on treatments for aging skin will be profound, and I'm eager to go into more detail. For now, though, we'll focus on the questions at hand: Just what is epigenetics? And, what does epigenetics have to do with skin cancer?
What do we mean by Epigenetics?
Epigenetics means literally 'on top of' genetics. It refers to heritable changes that are not actually encoded in the DNA, but nevertheless do play an important role in how your genes express themselves. For instance, epigenetics explains why a skin cell looks different from a muscle cell or a liver cell. Though all three cells contain the same DNA, their genes are expressed differently (turned 'on' or 'off'), turning them into very different types of cells. Some of the best-known epigenetic mechanisms that can switch genes 'on' or 'off' include DNA methylation, histone modifications and non-coding RNA.
Epigenetics and Skin Cancer
Now let’s go back to UV exposure and skin cancer and bring in the epigenetics piece of the puzzle. We know that in the initiation stage, UV exposure damages the DNA. This damage results in a cascade of events ranging from inflammation and erythema to sunburn. However, when excessive UV exposure overwhelms DNA repair capabilities epigenetic changes such as alterations in DNA methylation can occur. Results could mean altered gene expression, cell membrane damage, apoptosis (cell death) and a compromised immune system. This in turn can lead to all sorts of unwanted outcomes including immunosuppression, gene mutations and skin cancer.
There are many ways epigenetic changes promote skin cancer development. One example is a UV-induced mutation in the p53 tumor suppressor gene. Skin cells carrying the p53 mutation are resistant to apoptosis (cell death) and undergo clonal expansion that can lead to the formation of actinic keratoses (age spots) and squamous cell carcinoma.
It’s beginning to sound like the more we discover, the bleaker the outcome. However, there is a bright side—and it’s very bright indeed.
Here's the good news: Evidence accumulated over the past decade strongly suggests that diet and environmental factors directly influence epigenetic mechanisms in humans. We can have an impressive measure of control over how healthy we are, because while we can’t change our genes, we can influence how they are expressed.
Further study in epigenetics holds great promise in treating aging skin (stay tuned for future blog posts…), but important discoveries have already been made with respect to diet and skin cancer prevention. In particular, dietary polyphenols from green tea, turmeric and broccoli have been found to exert chemopreventive effects by regulating epigenetic mechanisms.
Sun Protection Tips
In addition to drinking green tea and eating your broccoli, you can wear it—literally. Look for green tea-based spray on mists or make one yourself. It’s easy and frugal. Drink your green tea, but don't throw away the tea bags. Let them steep overnight in filtered water—about one bag per cup of water. If you steam your broccoli or boil it in a bit of water add the remaining water to your green tea mixture. Keep the blended mist refrigerated.
Sun Protection Under a New Light—UVA Light, Part 4
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