Nat Com: sunburns provoke inflammation and skin cancer.
Excessive sun exposure can trigger a hidden mechanism that transforms normal skin cells into cancerous ones. Researchers at the University of Chicago have discovered that ultraviolet light destroys a key protein, YTHDF2 — an inflammation regulator that keeps cells in a normal state. The study is published in Nature Communications (Nat Com).
The scientists demonstrated that a decrease in YTHDF2 levels in cells significantly enhances inflammation caused by sunburn. This occurs because RNA molecules altered by UV begin to activate the TLR3 receptor, initiating a powerful inflammatory cascade associated with skin cancer development. Normally, YTHDF2 blocks this reaction, effectively acting as a "guard" of cellular tranquility.
The authors found that YTHDF2 interacts with a specific molecule, U6 snRNA, and together they enter endosomes — unexpected cellular structures for these RNAs. There, the protein prevents the onset of inflammation, but when it is lost, control disappears, and damaged skin enters a state of chronic inflammatory stress.
The discovery shows that skin cancer begins not only due to mutations but also due to a failure in the regulation of inflammation. The researchers believe that restoring the function of YTHDF2 or blocking dangerous RNA interactions with TLR3 could be a new approach to preventing the consequences of sunburns and reducing the risk of developing skin cancer.
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