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Researchers at the Wellcome Trust Centre for Gene Regulation and Expression at Dundee University have found two new targets that inactivate of nuclear factor kappa B (NFκB), a factor that induces transcription of proteins that render cells resistant to programmed cell death (apoptosis), causing angiogenesis, cell proliferation, tumour formation, metastasis and inflammatory diseases such as arthritis and Crohn’s disease. They are now are seeking partnerships to develop the new agents.
Inhibition of NFκB activity is an important target in the design of drugs against cancer. It is known that its anti-apoptotic properties of NFκB can be reversed by mechanisms involving tumour suppressors such as p53. The Dundee University researchers have now identified two new targets for cancer therapies – p14ARF and RFC. These targets inactivate NFκB, arrest tumour growth, induce apoptosis and prevent proliferation of damaged cells.
The researchers have shown that p14ARF suppresses NFκB transcriptional activity and acts as a p53-independent tumour suppressor. By binding to NFκB, ARF renders cells sensitive to apoptosis induced by tumour necrosis factor and induces cell death without causing DNA damage.
DNA manipulation experiments using plasmids encoding small fragments of RFC have highlighted the importance of RFC in the prevention of tumour growth.
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