The protein makes tumours more aggressive, helping them migrate to other organs, according to research.
Experiments on human cells and mice found turning it off stopped the disease in its tracks, opening the door to potential new treatments.
Lead author Dr Lisa Moris, of the University of Leuven in Belgium, said: “We were able to show the regulation of the AZIN1 gene is closely associated with the risk of the tumour spreading.
“What we can say is this finding applies to the patients we tested, who were followed up over a period of ten years, as well as our mouse and in-vitro models.”
She added: “We are currently looking at what exactly this gene does, to see if we can find a way of regulating it in real-life cancers. Opening a way to controlling whether tumours risk spread would be a significant step towards controlling prostate cancer.”
Her team based the finding on 44 “high-risk” men with tumours likely to spread, or metastasise – 19 of whose did.
A DNA analysis showed they had many more copies of the AZIN1 gene than the 25 others who were cured after treatment.
To test this, the researchers changed its activity in cells grown in the lab and rodents genetically engineered to develop prostate cancer. Reducing the activity, or expression, of the gene resulted in less spread.
Dr Moris said: “We need to do a lot more research on AZIN1 to see if the relation with metastases is generally applicable to prostate cancers.
“There are many different types and causes of prostate cancer so this finding is still a long way from any clinical application.”
It is also believed AZIN1 plays a role in other cancers, offering hope of developing a drug for multiple forms including those of the breast, bowel and lung.
In the UK, about 11,000 men die from prostate cancer every year.