GSE108177
Total RNA-seq of cancer cells with inhibition of DNA and/or histone methylation
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. Overall design: Total RNA-seq were performed in four human cancer cell lines (HCT116, HL60, MCF7 and HepG2) following DNA methylation inhibitor (5-aza-CdR) treatment or knockdown of individual H3K9me2/3 histone methyltransferases (G9a, SETDB1, SETDB2, SUV39H1 and SUV39H2), H3K27me3 (EZH2) or a scaffold protein TRIM28. Dual inhibition of DNA methylation and histone modifications were conducted after 5-aza-CdR treatment and knockdown of individual histone methyltransferases (G9a, SETDB1, SETDB2, SUV39H1, SUV39H2 and EZH2) and TRIM28.