Satellite ncRNAs are emerging as key players in cell and
cancer pathways.
Cancer-linked
satellite DNA hypomethylation seems to be responsible for the overexpression of satellite non-coding DNAs in several
tumors. FA-SAT is the major
satellite DNA of Felis catus and recently, its presence and transcription was described across Bilateria genomes. This
satellite DNA is GC-rich and includes a CpG island, what is suggestive of transcription regulation via DNA methylation. In this work, it was studied for the first time the FA-SAT methylation profile in cat primary cells, in four passages of the cat tumor cell line FkMTp and in eight feline mammary
tumors and the respective disease-free tissues. Contrary to what was expected, we found that in most of the
tumor samples analyzed, FA-SAT
DNA was not hypomethylated. Furthermore, in these samples the transcription of FA-SAT does not correlate with the methylation status. The use of a global demethylating agent,
5-Azacytidine, in cat primary cells caused an increase in the FA-SAT
non-coding RNA levels. However, global demethylation in the
tumor FkMTp cells only resulted in the increased levels of the FA-SAT small
RNA fraction. Our data suggests that DNA methylation of FA-SAT is involved in the regulation of this
satellite DNA, however, other mechanisms are certainly contributing to the transcriptional status of the sequence, specifically in
cancer.