Why we funded it
New therapies for prostate cancer are needed to address the
growing level of resistance to existing treatments. The pathway
Professor Bates and his team have identified is a completely new
way of blocking cancer growth, but is as yet untested in prostate
cancer. If they can successfully show that this pathway - the
splicing pathway - is effective in prostate cancer it can be used
to develop new drugs that target this pathway.
Scientific title
Alternative splicing as a novel drug for prostate cancer
Research project summary
Although there are only 20,000 human genes, they can generate
over 1 million different proteins because the messages they give
out are edited in many different ways. Professor Bates's
group has already found that a key protein involved in growing new
blood vessels within tumours, VEGF, is a gene that produces
different forms of message.
One of these VEGF messages encourages blood vessel growth into
tumours, another suppresses it. As prostate cancer
progresses, there is a switch towards the form that encourages
blood vessel growth, so feeding the tumour with nutrients and
oxygen. This project will study why this switch happens and
whether it can be prevented by manipulating two proteins, ASF and
SRPK1, which appear to control it.
Using prostate cancer cells cultured in the laboratory, rodent
models and samples of human prostate tumours the student working on
this project will manipulate these proteins to see whether this
causes the blood vessel suppressing form of VEGF to be produced in
cancer cells. If so, there are already chemicals that block
ASF and SRPK1 which could form the beginnings of a new therapy for
prostate cancer.
Professor Bates hopes that by the end of this project the
research will be at a stage for drug companies to further develop
these chemicals into effective treatments for advanced prostate
cancer.