DNA methylation and histone acetylation are epigenetic modifications that act as 
regulators of gene expression. DNA methylation is considered an important 
mechanism for silencing of retroelements in the mammalian genome. However, the 
methylation of human endogenous retroviruses (HERVs) is not well investigated. 
The aim of this study was to investigate the transcriptional potential of 
HERV-Fc1 proviral 5'LTR in more detail, and examined the specific influence of 
CpG methylation on this LTR in number of cell lines. Specifically, the role of 
demethylating chemicals e.g. 5-aza-2' deoxycytidine and Trichostatin-A, in 
inducing or reactivating expression of HERV-Fc1 specific sequences and the 
mechanisms were investigated. In our present study, 5-aza-dC is shown to be a 
powerful inducer of HERV-Fc1, and at the same time it strongly inhibits 
methylation of DNA. Treatment with this demethylating agent 5-aza-dC, results in 
significantly increased levels of HERV-Fc1 expression in cells previously not 
expressing HERV-Fc1, or with a very low expression level. The extent of 
expression of HERV-Fc1 RNAs precisely correlates with the apparent extent of 
demethylation of the related DNA sequences. In conclusion, the results suggest 
that inhibition of DNA methylation/histone deacetylase can interfere with gene 
silencing mechanisms affecting HERV-Fc1 expression in human cells.