Researchers at the University of Glasgow have discovered a new mechanism which controls the ability of cells to divide and multiply. The breakthrough has important implications for the development of drugs to combat cancer, which occurs when cell division goes out of control.
Dr Lorna Morris and Dr Elizabeth Allen, working under the direction of Professor Nick La Thangue in the Institute of Biomedical & Life Sciences,University of Glasgow, have been studying a cell protein called E2F which controls cell growth and division.
Their research identifies a complex of proteins* which activate E2F, thus initiating cell division. But if these control proteins are faulty and E2F is over-activated, excessive cell division takes place. This can lead to cancer.
"This is an important breakthrough" says Professor La Thangue, "because by understanding the natural mechanisms which regulate E2F, we can understand what is going wrong. This provides us with the opportunity to develop small molecule drugs which can arrest E2F activity and prevent tumour cell proliferation."
This research contributes to a larger programme of work identifying targets for drug development being carried out by Prolifix Ltd, the UK-based cell cycle company. Professor La Thangue is chief scientific officer of the company, which has a unique understanding of how the cell cycle is controlled in nature.
Failures or aberrations in the control of the cell cycle lie behind cancer and a number of other diseases. The race is on to develop custom-made drugs to compensate for the failures in the natural control mechanisms. Says Professor La Thangue: "The research teams working on this at the University of Glasgow are making a substantial contribution to our understanding of this vital area. The more information we have of how the process of cell cycle control works, the better placed we are to devise ways of intervening effectively when it goes wrong."
* The complex of proteins identified by the researchers are cyclin E-Cdk2 kinase and group known as p300/CBP.
Cite This Page: