Published on Dec. 4, 2001 in Proc Natl Acad Sci U S A volume 98(25).
PubMed ID: 11717408
In mammals, RNA editing by site-selective adenosine deamination regulates keyfunctional properties of neurotransmitter receptors in the central nervous system.Glutamate receptor subunit B is nearly 100% edited at one position (the Q/R-site),which is essential for normal receptor function. Its significance is apparent frommouse models in which a slightly reduced rate of Q/R-site editing is associated withearly onset epilepsy and premature death. Here we report that in tissues frommalignant human brain tumors, this editing position of glutamate receptor subunit Bis substantially underedited compared with control tissues. We also observealterations in editing and alternative splicing of serotonin receptor 5-HT(2C)transcripts. These changes correlate with a decrease in enzymatic activity of theediting enzyme adenosine deaminase acting on RNA (ADAR) 2, as deduced from analysisof ADAR2 self-editing. Our results suggest a role for RNA editing in tumorprogression and may provide a molecular model explaining the occurrence of epilepticseizures in association with malignant gliomas.