Faultless: Your skin's battle with open wounds and cancer

The San Andreas fault.
In our skin, fringes of cells meet to close a wound.
(picture credit: David Parker)

New research has revealed a connection between how our skin heals and the prevention of skin cancers.

In a paper published  two weeks ago in JCB, Jeremy Rotty and colleagues showed that keratin 6 (K6), a fibrous protein used to repair skin lesions, can also put the brakes on skin cells growing too quickly.

When the surface of your skin is scratched, the wound is quickly bridged by keratinocytes, cells full of K6 which migrate through the tissue and mesh together. Researchers found that K6, as well as providing scaffolding inside these cells, also attaches to and controls Src, a protein at the heart of the wiring for cell migration and growth.

It is here that a careful balance is struck. If there isn't enough Src activity inside a keratinocyte, it may not migrate at all, leaving wounds exposed. Too much Src, however, and the cells could migrate too far, growing into tumours. Skin cells lacking K6 to control Src activity have been shown to  produce aggressive cancers.

Keratinocytes actually roll into a wound
in the skin, like stones into a valley.
(picture credit: moonjazz)

The researchers from John Hopkins University, Baltimore, USA suggested that inside skin cancer cells K6 might be a “protective mechanism that maintains epithelial (skin surface) tumours in a ... less aggressive state".

What does this mean for me?

Future treatments for skin cancer might target the relationship between K6 and Src. A lack of K6 might also be looked for as a marker for predisposition to certain types of skin cancer.

What does this mean for science?

This is a great example of multi-tasking inside our cells. Keratin K6 can regulate both the structure and movement of keratinocytes. The relationship between K6 and Src  shows how important the inner-wiring of each individual cell can be to the overall tissue, where lesions need to be repaired despite the risk of cancer.

Reference:

Rotty, J., & Coulombe, P. (2012). A wound-induced keratin inhibits Src activity during keratinocyte migration and tissue repair The Journal of Cell Biology, 197 (3), 381-389 DOI: 10.1083/jcb.201107078