Researchers from Belgium and Germany have published new data on how vascular endothelial growth factor (VEGF) is instrumental in regulating skin cancer stem cells. The findings reveal a dual role for this molecule in the promotion of skin cancer stem cell growth and tumour progression, which may have significant implications for the prevention and treatment of various skin cancers.

A study funded in part by a European Research Council (ERC) Starting Grant of €1.6 million under the EU's Seventh Framework Programme (FP7) to support the CANCERSTEM (Stem cells in epithelial cancer initiation and growth) project, and made by researchers in Belgium, in cooperation with German colleagues, has found a dual role for the molecule VEGF in the promotion of skin cancer stem cell growth and tumour progression, which may have significant implications for the prevention and treatment of various skin cancers.

In particular, the European researchers found that VEGF, a molecule that normally promotes new blood vessel formation, is expressed at high levels by skin cancer stem cells. The team genetically removed the expression of VEGF by tumour cells, and discovered that skin cancer stem cells were quickly lost due to a defect in their renewable properties. This in turn triggered tumour regression. The receptor which binds VEGF, called Neuropilin-1, is also highly expressed by skin cancer stem cells, and is also required to promote cancer stem cell renewal and tumour growth, according to the researchers. They discovered that the Neuropilin-1 receptor plays a critical role during both cancer initiation and tumour growth. The team highlights that while VEGF signalling in endothelial cells is needed indirectly by tumours to maintain the tumour's blood supply, its production and signaling in cancer stem cells also directly promotes cancer stem cell renewal and tumour growth.

Thanks to this new discovery, and according to the scientists, the results have important implications for the prevention and treatment of different epithelial cancers, as new therapies blocking VEGF and/or Neuropilin-1 functions in cancer cells may be more effective for the treatment of certain cancers compared to the therapeutic strategies blocking VEGF function only in endothelial cells.