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Neuronal regulators offer potential targets for cancer
Date:3/19/2008

classical characteristic of cancer cells.

After uncovering this role, Westbrook used a technique called RNA interference (RNAi) to search for proteins that reduce REST levels. He reasoned that these proteins might promote tumor formation if expressed outside the nervous system.

The RNAi screen netted a known tumor promoter called ß-TRCP. Further genetic tests revealed that ß-TRCP binds directly to REST, tagging it for destruction. But REST must be primed with a particular molecule called phosphate for this interaction to occur.

"If we can prevent ß-TRCP from binding to REST, we may be able to treat certain tumors that display neuronal gene expression profiles," says Elledge, who is also a member of the HMS-Partners HealthCare Center for Genetics and Genomics and investigator with the Howard Hughes Medical Institute. "Such profiles are remarkably common in epithelial cancers, such as breast cancer and ovarian cancer."

"This discovery is particularly exciting because the scientific community knows how to target enzymes that add and remove phosphate groups from proteins with small molecules," says Westbrook. "Big pharmaceutical companies have devoted lots of resources to accomplishing this task."

Information about the interaction between ß-TRCP and REST might also aid researchers in the embryonic stem cell field.

"It's hard to control the differentiation of embryonic stem cells into specialized cells such as neurons," says Westbrook. "If one could prevent ß-TRCP from tagging REST for destruction, one could potentially keep embryonic stem cells from turning into neurons. Alternatively, one might be able to make neurons more efficiently by quickening REST destruction."


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Contact: Alyssa Kneller
public_affairs@hms.harvard.edu
617-432-0442
Harvard Medical School
Source:Eurekalert

Page: 1 2

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