In humans, 97% of the genome are non-coding and among those, nearly half of the sequences are derived from transposable elements. These elements, retrotransposons in particular, can shape the genome by replicating and moving around by “copy-and-paste” mechanism. Based on these properties, transposable elements provide an enormous reservoir of regulatory modules for gene networks in both normal and disease conditions. Recent studies have shown the close interrelationship between oncogene expression in multiple types of cancer and the aberrant reactivation of transposable elements, especially retrotransposons. However, study related to this linkage is particularly lacking in glioblastoma (GBM), one of the most aggressive and incurable cancers of the brain. Here, this study aims at elucida...[ Read more ]

In humans, 97% of the genome are non-coding and among those, nearly half of the sequences are derived from transposable elements. These elements, retrotransposons in particular, can shape the genome by replicating and moving around by “copy-and-paste” mechanism. Based on these properties, transposable elements provide an enormous reservoir of regulatory modules for gene networks in both normal and disease conditions. Recent studies have shown the close interrelationship between oncogene expression in multiple types of cancer and the aberrant reactivation of transposable elements, especially retrotransposons. However, study related to this linkage is particularly lacking in glioblastoma (GBM), one of the most aggressive and incurable cancers of the brain. Here, this study aims at elucidating the potential regulatory role of retrotransposons by dissecting GBM’s transcriptome and epigenome, using multiple epigenomic tools such as total RNA-seq and ATAC-seq. The results indicate the possible role of retrotransposons as putative promoters or enhancers that affect the expression of genes related to brain-specific oncogenic properties and invasive features in cancer. Taken together, these findings accent the potential roles of retrotransposons in GBM and may shed light on the underlying GBM etiology.