Our results show that decitabine alters Mecp2/MeCP2 expression at both the transcript and protein levels. Importantly, even minor changes in Mecp2 transcript expression led to nearly 2- to 3-fold altered protein expression, highlighting the biological significance of proper regulation of Mecp2 expression at the transcript levels. The observed correlation between the Mecp2/MeCP2 (total) and Mecp2e1/MeCP2E1 transcript/protein expression at D2 reinforces the concept that potential changes in Mecp2 transcript levels may reflect possible changes at the protein levels. However, the non-correlated Mecp2/MeCP2 (total) and Mecp2e1/MeCP2E1 transcript/protein expression at D8 indicates that decitabine withdrawal causes not only transcriptional but also, post-transcriptional regulation of MeCP2 expression, leading to reduced expression of MeCP2 (total)/MeCP2E1. One such post-transcriptional regulatory mechanism could be the action of micro-RNAs such as miR132, expression of which has been shown to be increased by 5-aza-2′-deoxycytidine/decitabine [63], and has the ability to repress MeCP2 expression [64].
