The researchers found that a fragment of collagen VII is required for the skin cancer cells to break free from the neighboring skin tissue and spread – a step that turns an otherwise benign tumor into a killer. When this sequence was blocked, the cancer was also blocked from spreading.
The group found this sequence by studying skin samples from 12 children with a blistering skin disorder called recessive dystrophic epidermolysis bullosa (RDEB), which is caused by a mutation that leads to an altered or missing collagen VII protein.
The researchers deduced that a collagen VII protein fragment might be necessary to allow cancer to form. They proved this by adding the fragment to RDEB cells that lacked it – an intervention that restored cancer-forming ability.
Further proof came from work in normal skin cells. The group blocked that protein fragment using an antibody and once again tried to induce the cells to become cancerous. They failed as, without that fragment, the cancer could not spread.
Furthermore, it appears that the antibody blocks only the cancer-spreading aspect of collagen VII. The protein is still able to perform its normal job of keeping the skin intact.
Researcher Dr Paul Khavari said he could imagine a drug that blocks the collagen VII fragment being used pre-emptively to prevent skin cancer from spreading in people who are highly susceptible, such as children with RDEB or people who are chronically immune suppressed due to organ transplantation.
Despite this optimism, Khavari cautions that many further experiments are needed before this work could lead to any cancer treatment.