How does the anti-cancer molecule p53 get turned off?
- Researcher: Professor Neil Perkins
- Institution: University of Newcastle
- Award Amount: £180,479 for 3 years from July 2013
- Cancer Type: General Cancer Research
The NF-kappaB family of proteins are switched on by stress signals and help the cell adapt to threats from the environment and infection. They have an important role in regulating our immune system and inflammation. NF-kappaB proteins are also found to be incorrectly switched on in many types of cancer, meaning the active form can have cancer-promoting properties, including turning off the anti-cancer molecule p53. In response to cell stresses, chronic inflammation or genetic alterations there are two main communication pathways that can lead to the switching on of NF-kappaB. Communication pathways are similar to a line of dominoes. As one ‘domino’ falls, the message gets passed from one molecule, to the next until it reaches the final one, who then gets switched on and performs a task. However, if a domino is removed or falls at the wrong time this can lead to the wrong message being communicated and this can lead to cancer. Professor Perkins has recently found a new mechanism, which helps regulate one of these NF-kappaB communication pathways. This pathway allows NF-kappaB to switch off the anti-cancer molecule p53, which can prevent damaged cells from entering a dormant state. Entering this dormant state provides a mechanism for normal cells to escape becoming cancer cells. Professor Perkins will be using his Worldwide Cancer Research grant to investigate this mechanism in more detail. He hopes that by learning more about it we can prevent NF-kappaB switching off p53 and so find a way to treat the cancers in which this pathway has been activated.
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