"Prostate cancer could be 'halted' by injections," reports The Independent. While this headline rather simplifies the research findings, the research it's based on demonstrates an interesting way to stop prostate cancer – for mice, at least...
"Prostate cancer could be 'halted' by injections," reports The Independent.
While this headline rather simplifies the research findings, the research it's based on demonstrates an interesting way to stop prostate cancer – for mice, at least.
In the research, mice with a "model" of prostate cancer were treated with chemicals that inhibit a protein called SRPK1. As a result, the growth of their cancer was reduced.
The researchers performed additional experiments, which showed SRPK1 is involved in the control of how new blood vessels grow. Blood vessels are required to bring oxygen and nutrients and remove waste, which is thought to be key for tumour growth.
Without SRPK1, blood vessel formation was reduced – suggesting that this could "starve" the tumours (as the Mail puts it) of food and oxygen.
Interestingly, this study suggests SRPK1 inhibitors may be used to treat prostate cancer, and potentially some other forms of cancer.
Because this has only been tested on mice, we have no way of knowing if the treatment will be safe for men with prostate cancer, let alone more effective than other treatments currently available.
Where did the story come from?
The study was carried out by researchers from the University of Bristol, North Bristol NHS Trust, the University of the West of England and the University of Nottingham.
It was funded by Prostate Cancer UK, the Biotechnology and Biological Sciences Research Council, the Medical Research Council, Cancer Research UK and the Richard Bright VEGF Research Trust.
The study was published in the peer-reviewed medical journal Oncogene.
The media reporting was generally accurate, although the headlines might be construed as misleading, as they seem to imply that a new prostate cancer treatment is available.
But these headlines are based solely on the results of experiments on cells grown in the laboratory and on mice. We'll have to wait and see if the proposed therapy is safe and effective enough to treat men with prostate cancer.
What kind of research was this?
This was a laboratory and animal study that built on the results of previous research.
Blood supply is required to bring oxygen and nutrients, and remove waste from tissues – including tumour tissue. The growth of new blood vessels (known as angiogenesis) is believed to be essential for tumour growth.
Angiogenesis is caused by the protein vascular endothelial growth factor (VEGF). However, a different form of the protein can be made in a process called splicing, which does the reverse and actually inhibits the growth of new blood vessels.
The researchers recently found the choice of "form" of VEGF is controlled by another protein called SRSF1.
When SRSF1 is modified by another protein called SRPK1, it favours the formation of the form of VEGF, which promotes the formation of new blood vessels. When it is not modified, it favours the formation of the form of VEGF that inhibits the growth of new blood vessels.
In this study, the researchers wanted to see whether:
- levels of SRPK1 or SRSF1 are increased in prostate cancer cells
- modification of the VEGF form produced is able to reduce tumour growth in animals
They wanted to see if there was potential for SRPK1 inhibitors to be used as a prostate cancer treatment.
What did the research involve?
The researchers first looked at the levels of SRPK1 and SRSF1 in 17 human prostate cancer samples.
They then performed a series of experiments on prostate cancer cells grown in the laboratory.
Following this, they looked at the growth of the prostate cancer cells injected into mice.
What were the basic results?
The researchers found levels of both SRPK1 and SRSF1 were higher in malignant (cancerous) areas compared with benign (non-cancerous) areas in the 17 human prostate cancer samples they examined.
When the researchers modified prostate cancer cells so they didn't make SRPK1, they found cells then made more of the form of VEGF that inhibits the growth of new blood vessels. However, the cells were still able to grow, divide and move as normal.
The researchers then injected the prostate cancer cells (either unmodified, or modified so they didn't make SRPK1) into mice. The researchers found the modified prostate cancer cells grew slower, formed smaller tumours, and had fewer blood vessels.
The researchers then did experiments with chemical inhibitors of SRPK1. They found the chemical inhibitors had similar effects to modifying the cells so they didn't make SRPK1.
When mice with a model of prostate cancer were treated with injections of chemical inhibitors of SRPK1, the growth of tumours was inhibited.
How did the researchers interpret the results?
The researchers say the results suggest that, "modulation of SRPK1 and subsequent inhibition of tumour angiogenesis by regulation of VEGF splicing can alter prostate tumour growth, and supports further studies for the use of SRPK1 inhibition as a potential anti-angiogenic therapy in prostate cancer".
In this study, researchers have found treating a mouse model of prostate cancer with chemicals that inhibit a protein called SRPK1 reduced cancer growth.
The researchers performed additional experiments, which showed SRPK1 is involved in the control of angiogenesis (the growth of new blood vessels). Blood vessels are required to bring oxygen and nutrients, and remove waste from tissues.
The formation of new blood vessels is thought to be key for tumour growth, and without SRPK1, blood vessel formation was reduced.
This study has suggested SRPK1 inhibitors could be used to treat both prostate and other forms of cancer. However, this study only trialled the potential therapy in mice.
Further studies are needed to show that the treatment is safe for men with prostate cancer. If that is confirmed, more work will be needed to show it is effective in treating men with prostate cancer.
Analysis by Bazian. Edited by NHS Choices. Follow Behind the Headlines on Twitter. Join the Healthy Evidence forum.