Related Experiment Video
Updated: Mar 3, 2026

Investigation of the Transcriptional Role of a RUNX1 Intronic Silencer by CRISPR/Cas9 Ribonucleoprotein in Acute Myeloid Leukemia Cells
Published on: September 1, 2019
Transposable Elements in Human Cancer: Causes and Consequences of Deregulation
Sumadi Lukman Anwar1,2,3, Wahyu Wulaningsih4,5,6, Ulrich Lehmann7
1Division of Surgical Oncology, Department of Surgery Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta 55281, Indonesia. sl.anwar@ugm.ac.id.
Abstract:
Transposable elements (TEs) comprise nearly half of the human genome and play an essential role in the maintenance of genomic stability, chromosomal architecture, and transcriptional regulation. TEs are repetitive sequences consisting of RNA transposons, DNA transposons, and endogenous retroviruses that can invade the human genome with a substantial contribution in human evolution and genomic diversity. TEs are therefore firmly regulated from early embryonic development and during the entire course of human life by epigenetic mechanisms, in particular DNA methylation and histone modifications. The deregulation of TEs has been reported in some developmental diseases, as well as for different types of human cancers. To date, the role of TEs, the mechanisms underlying TE reactivation, and the interplay with DNA methylation in human cancers remain largely unexplained. We reviewed the loss of epigenetic regulation and subsequent genomic instability, chromosomal aberrations, transcriptional deregulation, oncogenic activation, and aberrations of non-coding RNAs as the potential mechanisms underlying TE deregulation in human cancers.
More Related Videos
Related Concept Videos
Non-LTR Retrotransposons
Epigenetic Regulation
X-chromosome...
Epigenetic Regulation
Overview of Transposition and Recombination
Induced Pluripotent Stem Cells
Somatic...
Cancer-Critical Genes I: Proto-oncogenes
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...

