Skin tumour reduced in mice
Squamous cell skin carcinoma is the second most common skin cancer after melanomas, affecting approximately 10,000 people in the UK each year. Previous research has shown that this form of cancer, and several others, relies on cancer stem cells. These lie under the skin near blood vessels and are able to continuously divide providing cells to grow the tumour at the skin surface. Now scientists have uncovered a signalling pathway that allows skin tumours to grow. By blocking the pathway they were able to shrink tumours in mice. The work could lead to new ways to treat the disease as there are already medicines designed to block the receptors involved.
Researchers investigated the role of a signalling molecule called VEGF and its receptor found on cells under the skin. Scientists already know that this signalling pathway plays an important role in the formation of new blood vessels to feed fast-growing tumours. Medicines already exist that block the receptor on blood vessels, but the researchers were interested in the effect of VEGF on cancer stem cells.
Using an antibody designed to block the cell-receptor for VEGF the scientists not only prevented new blood vessels forming but also stopped cancer stem cells from dividing. This caused skin cancer tumours in mice to shrink. This suggested that VEGF is a signal molecule for cancer stem cells to multiply.
Using cancer stem cell line in culture they then identified a protein, called neuropilin-1, which is associated with the VEGF receptor specifically in cancer stem cells. When neuropilin-1 was genetically deleted VEGF molecules binding to their receptor had no effect and so the cancer stem cells didn't multiply.
Further work can now be done to modify existing chemotherapy treatments to block this newly characterised pathway.