Researchers studying cancer epigenetics therapies dream of days when we might be able to control DNA methylation like our car stereos…less treble, little more bass. 5 Aza is one of the early leaders in the epi pipeline, and like a lot of therapeutics out there, we learn more about how it impacts other cellular processes frequently.
The cytosine analog azacytidine has already been FDA approved to treat preleukemias, and is being investigated for other neoplasticities as well — both alone and in combination with HDACs. It stops up the works of DNA methyltransferases, leading to passive DNA hypomethylation over several replication cycles.
But, according to a group from the German Cancer Research Center in Heidelberg, azacytidine might actually be more potent at inhibiting the methylation of RNA than it is of DNA. They looked at various cancer cell lines in which the DNA methyltransferase DNMT2 – which has known RNA methyltransferase activity – is expressed, and found that azacytidine induces hypomethylation of specific target sites on tRNA at far lower titers than it does on its DNA targets.
See how this might lead to better biomarker ID and other wonders at Cancer Research, October 2009