It’s not news that miRNAs are out of whack in cancers. So it shouldn’t be surprising that re-expressing an oncogene-targeting miRNA might halt tumor progression. But what if the miR didn’t even have to target a specific oncogene to show off its anti-proliferative mojo? Son and father research duo (we’re pretty sure they dominated the school science fair), Joshua and Jerry Mendell set out to get away from all the specifics and see if miRNAs could be used as general anticancer agents.
In work featured tomorrow in Cell, they looked at mice transgenic for hepatic expression of MYC. These mice get liver tumors that look like hepatic carcinoma (HCC), and downregulate a host of miRNAs including miR-26a. Transfecting mice with the miR-26a gene — using an AAV vector, which targets the liver – resulted in cancer cell cycle arrest and apoptosis, and protected the animals from disease progression. Normal tissue seemed to be unaffected.
Although miR-26a targets cyclin D2 and E2 mRNA, it doesn’t faze Myc mRNA. The Mendells aren’t exactly sure yet how just restoring miR-26a expression stops the cancer without targeting the initiating oncogene, but they offer up some solid thoughts that you can check out in Cell, June 2009