Endogenous Retroviruses (ERVs) silencing mechanism depend on DNA methylation, heterochromatin conformation and the PRC2 complex. However, extensive maps of ERVs distribution and the associated epigenetic marks have not yet been provided in human cancer cells. Our purpose in this study is to investigate ERVs expression changes after inhibition of DNA and/or histone methylations. Total RNA-seq in human colon cancer HCT116 cells following DNA methylation inhibitor treatment or knockdown of individual H3K9me2/3 histone methyltransferases revealed that about 1,000 of evolutionary young ERVs were predominantly silenced by DNA methylation, whereas about 800 of intermediate age ERVs were silenced by histone methylations. ERVs therefore have undergone an epigenetic switch in silencing mechanism during host genome evolution. SOURCE: Peter,A,Jones (Peter.jones@vai.org) - Jones Lab Van Andel Research Institute

Pluto Bioinformatics

GSE108177: Total RNA-seq of cancer cells with inhibition of DNA and/or histone methylation