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Notorious cancer gene may work by destroying messenger

COLUMBUS , Ohio A new study suggests how a notorious cancer gene may contribute to tumor growth.

The insight emerged from a long-running study of a protein called PMR1, the key player in an unusual mechanism that cells use to quickly stop production of certain important proteins.

Researchers discovered that PMR1 is activated or turned on by another molecule, an energy-packing protein called Src (pronounced sark).

Discovered in 1977, Src became the first oncogene mutated genes that help make cells cancerous. Oncogenes are altered forms of genes that control cell growth and cell division.

These findings provide insight into how Src might contribute to cancer development.

The study by researchers with the Ohio State University Comprehensive Cancer Center is published in the March 9 issue of the journal Molecular Cell.

The link between Src and cancer was discovered 30 years ago, but to this day, we still don't know its exact role in tumor development, says principal investigator Daniel R. Schoenberg, professor of molecular and cellular biochemistry.

Our data suggest that Src may promote cancer by causing PMR1 to halt production of proteins that normally put the brakes on cell growth tumor-suppressor proteins, for example, or other growth-regulating proteins.

In healthy cells, Src helps control cell proliferation, differentiation, survival and movement. Mutated Src is found in about half of all colon, liver, lung, breast and pancreatic tumors, and the amount of Src can be significantly higher in cancer cells compared to normal cells.

Earlier research led by Schoenberg found that PMR1 helps control protein production by destroying particular messenger RNAs (mRNAs), molecules that carry the information used to assemble a protein.

That work showed that PMR1 attaches to the mRNAs and remains there as a silent passenger. If it receives the proper signal, howev
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Contact: Darrell E. Ward
Darrell.Ward@osumc.edu
614-293-3737
Ohio State University
19-Mar-2007


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