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Once given 'no respect,' cells' tiny RNAS take driver's seat

effects.

"So the Myc protein 'turns up' the genes for E2F1 and the microRNAs, but the microRNAs reduce the amount of E2F1 protein that can be made, fine-tuning Myc's effects, perhaps," says Mendell. "We chose to look for interactions with E2F1 specifically, but there are bound to be many, many more genes that these microRNAs regulate."

"Whether too much or too little of these or other microRNAs is a good thing or a bad thing -- whether it would contribute to or help prevent cancer -- depends on their targets in the cell," adds Myc specialist Chi Dang, M.D., Ph.D., the Johns Hopkins Family Professor in Oncology Research and a professor of medicine in the McKusick-Nathans Institute and the Johns Hopkins Kimmel Cancer Center. "Slowing E2F1 production would seem to be a good thing because doing so would slow cell growth, but that might not be the case for other genes controlled by these microRNAs."

Encoded for by genes' DNA, just like other RNA, microRNAs start out more than 1,000 building blocks long. Because they are able to fold back on themselves, they form double-stranded RNA, rather than the single strand characteristic of messenger RNA. As a result, the cell breaks the RNA into pieces. All sections except the microRNAs, just 21 to 23 building blocks long, is discarded.

The microRNAs can bind to single-strand messenger RNAs of the right sequence, which at the very least interferes with their ability to be read to make proteins and sometimes leads to the RNAs' destruction.

"Now we're figuring out the functions of these Myc-controlled microRNAs, other genes they regulate, and how else they might be involved in Myc-mediated initiation of cancer," says O'Donnell, who conducted her graduate work in Dang's laboratory.


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Source:Johns Hopkins Medical Institutions


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