A new treatment tested in mice could stop prostate tumors in their tracks.
Researchers found a specific compound can inhibit the activity of a molecule that allows tumors to form new blood vessels, which are essential for the survival of cancer cells, the University of Bristol reported. The molecule, called SRPK1 could stop the progression of prostate tumor growth.
"There's no denying that there are too few treatment options for the 40,000 men that face a diagnosis of prostate cancer every year in the UK - especially for those with advanced disease. Prostate cancer continues to kill over 10,000 men annually and there is an urgent need for new treatments if we are to significantly reduce this figure," said Matthew Hobbs, Deputy Director of Research at Prostate Cancer.
The blood vessel-forming process of angiogenesis is regulated by vascular endothelial growth factor (VEGF), which can either activate or inhibit blood vessels depending on how the gene is controlled by a cellular process called "alternative splicing."
The researchers found SRPK1 increases as the cancer gets more aggressive.
"We reasoned that inhibition of SRPK1 activity could stop cancer progression. Indeed, we show in this paper that if we decrease SRPK1 levels in prostate cancer cells, or in tumours grafted into mice, we are able to switch VEGF splicing and therefore inhibit tumour vasculature and growth."said Dr. Sebastian Oltean, the study's co-author from the University of Bristol's School of Physiology and Pharmacology,
The research team was able to decrease the tumor growth in a mouse model of prostate cancer though three weekly injections of the SRPK-blocking drug called SPHINX.
"Although it's early days, each finding like this represents a crucial block in building up our understanding of what can slow down and stop the progression of prostate cancer. This understanding will give us the foundations needed to develop new targeted treatments for those men in desperate need," Hobbs concluded.
The findings were published Nov. 10 in the journal Oncogene.
