Cancer Research UK scientists have unravelled a last resort ‘survival tactic’ that helps cells combat DNA damage, the trigger for cancer.
The discovery, published today (Thursday 16th June 2005) in Cell, gives researchers an important insight into the mechanisms human cells use to ensure their genetic code is correctly deciphered into instructions for life. It also provides a basic understanding of what might go wrong to lead to human diseases, such as cancer.
During normal growth, a cell’s DNA can become damaged. If the damage is not repaired, the cell is usually destroyed, but, sometimes this doesn’t happen, and the damage allows the faulty cell to reproduce uncontrollably and develop into cancer.
Now scientists, based at Cancer Research UK’s London Research Institute, have discovered that damaged cells employ a last resort tactic to ensure efficient deciphering of the genetic code and to enable DNA repair to take place.
In cells with DNA damage, the machinery that ‘reads’ the cell’s genetic code gets stuck at the damage, preventing the code from being deciphered and potentially leading to cell death. This new research shows that cells deal with this problem by specifically ‘tagging’ the stuck machinery for rapid destruction. This ‘clears’ the block so that DNA can be repaired and deciphered correctly.
Lead researcher, Dr Jesper Svejstrup, based at Cancer Research UK’s London Research Institute, says: “Our work unravels one of the very basic mechanisms cells use to combat DNA damage that can occur during normal growth or upon exposure to UV-light and certain chemicals. This is important to understand because, without it, substantial cell death would result from any exposure to DNA damaging agents and the surviving cells could begin to divide uncontrollably and develop into cancer.”
Professor John Toy, Medical Director at Cancer Research UK, says: “Any insight into how the body defends itself against cancer is important if we’re to find new ways to prevent and treat the disease. This research is at the basic biology level increasing our understanding of what controls normal cell behaviour.”
Baggavalli P. Somesh, James Reid, Wei-Feng Liu, T.Max M. Sogaard, Hediye Erdjument-Bromage, Paul Tempest, and Jesper Q. Svejstrup. Multiple Mechanisms Confining RNA Polymerase II Ubiquitylation to Polymerases Undergoing Transcriptional Arrest” Cell (2005)
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