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Understanding a new target to slow the growth and spread of prostate cancer

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Professor Joanne Edwards

Grant information

Institution - University of Glasgow
Researcher - Professor Joanne Edwards
Grant award - £130,220
Duration - 2011-2013
Reference - PG10-15 Edwards

We have identified that patients with STAT1 loss have a poorer prognosis. Further understanding of its role in prostate cancer development and progression could lead to STAT1 becoming a target for treatments.
Professor Joanne Edwards

Why did we fund this project?

  • Cancers, such as prostate cancer, form when cells start to multiply uncontrollably. To prevent this, cells produce tumour suppressors, that act as an ‘emergency brake’ to stop the cells multiplying too much.
  • When cells develop into cancer, they often stop producing these tumour suppressors, releasing the brake, and allowing the cancer cells to multiply quickly.
  • Professor Joanne Edwards and team had previously uncovered a new potential tumour suppressor called STAT1. They showed that prostate cancer cells which multiply and spread quickly stop producing STAT1.
  • In this project, the team wanted to confirm that STAT1 is an important tumour suppressor in prostate cancer in men, and understand the mechanism that allows it to 'put the brakes' on prostate cancer.
  • This could identify targets for new drugs that could put the brake back on, and slow the growth and spread of prostate cancer.
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What did the team do?

  • The team studied whether the amount of STAT1 in men’s prostate cancer was linked to how quickly their cancer grew, spread, and came back after treatment.
  • They also used prostate cancer cells grown in the lab to study STAT1 closely, to identify exactly how it ‘puts the brake’ on prostate cancer growth and spread, and which other targets it interacts with to do this.

What did the team achieve?

  • The team showed when men’s prostate cancer stops producing STAT1, it grows and spreads more quickly, and comes back sooner after treatment.
  • The team found STAT1 interacted closely with another target called SOCS3. Prostate cancers that stop producing both these targets grow and spread even quicker. This suggests they could both be important components of the ‘brake’.
  • The team found STAT1 production was also linked to the amount of inflammation in the tissue surrounding the cancer. This is important as inflammation is known to play a role in the development and spread of prostate cancer.

What does this mean for men?

  • This work has shown that STAT1 could be a key tumour suppressor, providing a 'brake' on prostate cancer growth and spread.
  • This suggests STAT1 could be targeted by new treatments to 'put the brake back on' and slow the growth and spread of prostate cancer.
  • Researchers are now studying STAT1 and the other targets it interacts with more closely, to understand how best to target it with a new drug.
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