Professor Nicholas La Thangue and his team at the Institute of Biomedical and Life Sciences at the University of Glasgow have unlocked the crucial communication pathways of p53 protein, which could ultimate aid the slowing down of cells that cause tumours and related disease.

A paper published this week in Nature Cell Biology online, explores how normal cells grow and divide in a tightly regulated fashion. This fine balance is achieved through molecular pathways that act inside cells and function as accelerators or brakes. In cancer, genetic mutations in certain key genes (caused for example through smoking) alter the activity of these pathways, so that the accelerators remain permanently on, and the brakes are continually off. These molecular changes unleash the unregulated and continual growth which is characteristic of tumour cells.

A crucial pathway that in normal cells blocks the appearance of tumour cells involves a protein called p53. This is one of the key braking mechanisms, although the details of how p53 is controlled (ie. how the braking mechanism is switched on) remain elusive. The topic of the current study delves in to this important subject and has uncovered the mechanism that controls p53 activity. It turns out that a novel protein factor, called Strap, acts as a linchpin in the p53 response. Essentially, Strap communicates with p53, and this needs to happen for cells to stop growing. The signals which Strap receives during this process are detailed in the study. Most interestingly, in some diseases where the patients suffer from a high incidence of cancer, we have found that the Strap protein is not controlled in the right way, which more than likely contributes to progression of tumours in these patients.

'An important point is that, because we now have a clear molecular understanding of how this critical pathway goes wrong, we can devise drugs that target, and correct, the defect,' explains Professor La Thangue.

'We believe that these drugs would be ideal cancer drugs because they would, in effect, reinstate the brakes in tumour cells and thereby stop them growing.'

For more details see: Nature Cell Biology Online.

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First published: 20 September 2004