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KEAP1 Keeps major cancer-promoting protein at bay
Date:10/9/2009

emonstrated that the presence of KEAP1 inhibits the NF?B signaling pathway and then conducted a series of experiments to find out how that happens. They found that depletion of KEAP1 leads to the accumulation of IKK, and then discovered that the tumor suppressor binds to a specific site on IKK, capturing it to feed it to the proteasome.

Hung likens this snatching of IKK to plucking stuffed animals with a mechanical claw out of an arcade game, imagery that wound up on the cover of Molecular Cell.

KEAP1 is a ubiquitin ligase that attaches to the target protein and works in a complex with another protein, CUL3, that connects the ubiquitins to the bound protein.

The team analyzed both KEAP1 and CUL3 expression in the tumors of 119 breast cancer patients and correlated the findings to overall survival. They found that underexpression of KEAP1 alone was associated with poor survival. Patients with strong expression of both KEAP1 and CUL3 had an 80 percent survival rate at five years while those with little expression of either had a 43 percent 5-year survival rate.

Next, they sequenced KEAP1's genes in 26 cancer lines (18 breast, four liver, four lung) and in 119 primary tumors (17 breast, 78 liver, 13 lung, 11 colon) and found two functional genetic mutations that shut down the protein's ability regulate IKK. The mutations affected the portion of the protein that binds to IKK.


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

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