Targeting a single molecule may stop prostate cancer in its tracks
In the spread of prostate cancer, one particular molecule is critical. Called SRPK1, it enables a tumor to generate new blood vessels and start to grow. Research conducted at the University of Bristol shows that a specific compound can thwart its activity, potentially leading to new forms of treatment for the disease.
A process called angiogenesis, in which the SRPK1 molecule is pivotal, sees the formation of new blood vessels in a tumor. The vessels then provide the nutrients the tumor needs to survive and flourish. Angiogenesis is regulated by vascular endothelial growth factor (VEGF), which either initiates or inhibits the vessel formation depending on a cellular process called alternative splicing.
The Bristol researchers studied samples of human prostate cancer, finding that levels of SRPK1 rose as a cancer becomes more aggressive.
"We reasoned that inhibition of SRPK1 activity could stop cancer progression," says Dr Sebastian Oltean, the study’s co-author from the University of Bristol’s School of Physiology and Pharmacology.
The researchers injected mouse models of prostate cancer three times per week with drugs designed to inhibit SRPK1 activity.
"Indeed, we show in this paper that if we decrease SRPK1 levels in prostate cancer cells, or in tumors grafted into mice, we are able to switch VEGF splicing and therefore inhibit tumor vasculature and growth," he continues.
A biotech company called Exonate is now looking to develop SRPK1 inhibitors with a view to treating diseases with abnormal vessel development such as age-related macular degeneration and cancer.
"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," says Dr Matthew Hobbs, Deputy Director of Research at Prostate Cancer UK. "This understanding will give us the foundations needed to develop new targeted treatments for those men in desperate need."
The research was published in the journal Oncogene.
Source: University of Bristol