‘Distress beacon’ drives inflammation in skin cancer
Worldwide Cancer Research funded scientists have located the molecular ‘distress beacon’ damaged skin cells use to attract immune cells during inflammation. These recently published findings could help scientists find a new way to target inflammation-driven cancer. And that’s great, but if you’re not really sure what inflammation actually is, and what it has to do with cancer-then read on!
Inflammation and cancer
We all know what inflammation looks like. If you’ve ever felt the red, warm, puffiness surrounding an insect bite or a new graze or cut, or even had a cold and a sore throat, chances are part of what you felt was due to short-term, localised inflammation of your tissues.
Inflammation is the influx of immune cells and special factors to a part of the body in ‘danger’. It’s part of our immune system’s first-response to outside irritants, barrier breakdowns, and invaders such as bacteria or viruses. Short-term inflammation is essential to our survival. It helps wounds heal, and clears infections.
But for various reasons inflammation can also sometimes stick around in the body, developing into self-sustaining or chronic, long-term, inflammation. This might be because the infection or irritant persists for a long time, for example. Or because the immune system has accidentally picked on something that is not a harmful invader but is instead a healthy part of the body (an autoimmune response).
It is this chronic inflammation which can be a major risk factor for many types of diseases, including some cancers.
Scientists actually think that with certain types of long-term inflammation, the immune cells might inadvertently start helping damaged cells which should die off to survive. These damaged cells can then keep dividing, signalling the start of a dangerous process- and making way for cancer to develop.
But scientists don’t well understand why the immune cells feel compelled to come and help these damaged cells in the first place.
What did the scientists do?
Dr Cathy Tournier and her team at the University of Manchester have now pieced together a part of that puzzle. They studied mice with inflammation-driven skin cancer and found that one molecule, called ERK5, acts like a ‘distress beacon’ for damaged skin cells. It seems that in times of trouble, the damaged cells can use ERK5 to draw in immune cells from afar.
“We think it’s quite clear,” says Dr Tournier, “our work shows the skin cells are using ERK5 to ‘call’ to the immune cells.”
The team then went further - and gathered crucial evidence which suggests that blocking ERK5 from sending out the distress signals might slow skin tumour development. They also showed that this effect helped boost the action of low doses of the chemotherapy drug doxorubicin. This suggests that targeting ERK5 might even be a new way to approach treating cancer.
There’s a long way to go, but we think that anti-ERK5 therapy combined with chemotherapy might turn out to be an effective way to hit not just skin cancer, but maybe many different types of cancer, said Dr Tournier.
So what’s next?
“This research was done in mice so we don’t yet know what these findings mean for humans,” explains Dr Helen Rippon, Head of Research at Worldwide Cancer Research. “But it’s a great step forward, and early-stage research like this is vital if we are going to continue making the huge advances in cancer survival we’ve already seen over the last few decades.”
And Dr Emma Smith, Senior Science Information Officer at Cancer Research UK, who also supported the study, said: "Discovering more about the molecules that control inflammation could help to develop new treatments that dampen it down, which might slow the growth and spread of cancer."
Worldwide Cancer Research has just awarded Dr Cathy Tournier a new grant to continue her exciting work in this area, so watch this space!
This research was funded by Worldwide Cancer Research and Cancer Research UK.
Thank you to Dr Patrick Caswell for his microscope image of invading cancer cells.