MicroRNAs are made by the same cellular machinery that makes other forms of RNA -- like the messenger RNA used to build proteins. However, microRNAs are immediately processed by cellular machinery that deals with what is known as RNA interference -- a biological phenomenon that specifically prevents RNA from being used to make proteins.
Accompanying the Hopkins paper are two reports looking specifically at microRNAs in cancer -- one in humans, one in mice. One report shows that human tumors' microRNA "fingerprints" -- patterns showing which of the more than 200 known microRNAs are more or less abundant than normal -- identify the tumors' tissue of origin much better than other tests. The other paper shows that over-expression of chromosome 13's microRNAs dramatically increases the risk of cancer in mice predisposed to cancer because of a faulty Myc gene.
"We've found that there's complex crosstalk between Myc, the microRNAs and the genes that both control," says Mendell. "This complex system, if disturbed, has the potential to very potently drive cell growth and cancerous proliferation."
Among the genes Myc controls is one called E2F1, which, like Myc, also controls the expression of genes. One of the genes controlled by E2F1 just happens to be the gene for Myc.
"This establishes a feedback loop," says Kathryn O'Donnell, Ph.D., who conducted much of the work as a graduate student in the Human Genetics Program. "Because both Myc and E2F1 increase the expression of genes that increase cell growth, the pair could be quite dangerous if they simply fed off each other."
But the researchers also discovered that two of the six microRNAs controlled by Myc actually reduce cells' ability to use E2F1's protein-building instructions. Essentially, these microRNAs act as a "brake" to slow E2F1's growth-promoting
Source:Johns Hopkins Medical Institutions