THESIS
2021
1 online resource (viii, 72 pages) : illustrations (chiefly color)
Abstract
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...[
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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.
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