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Pathway links inflammation, angiogenesis and breast cancer
Date:8/13/2007

following NF"B into the nucleus, where IKKa plays the pivotal role in the oncogene's competition with the tumor-suppressing gene p53 for access to CREB-binding protein (CBP).

Both p53 and NF-kB covet CBP, an extremely popular activator of genes that interacts with hundreds of other proteins, Hung notes. In the case of the tumor suppressor and the oncogene, CBP will bind to only one at a time.

"You can think of them as a good guy, and a bad guy, with a gun lying between them. Who gets the gun" And how does one get it"" says Hung.

Hung and colleagues showed that IKKa phosphorylates CBP in the nucleus, switching CBP's binding preference to the NF"B oncogene, promoting cell growth. Unphosphorylated CBP helps p53 do its job suppressing cancer by forcing defective cells to kill themselves, programmed cell death known as apoptosis.

"If you can control IKKa, you get a double-dip effect," Hung says. "You not only activate p53, the good guy, you keep the bad guy out of the contest."

IKKa and IKK together help NF"B escape into the nucleus, where it promotes cell growth and blocks programmed cell death. IKKa then works separately in the nucleus and IKK in the cytosol to induce cancer through separate pathways.


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Contact: Scott Merville
sdmervil@mdanderson.org
713-792-0661
University of Texas M. D. Anderson Cancer Center
Source:Eurekalert

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