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Int J Mol Sci. 2017 May 4;18(5). pii: E974. doi: 10.3390/ijms18050974.

Transposable Elements in Human Cancer: Causes and Consequences of Deregulation.

Author information

1
Division of Surgical Oncology, Department of Surgery Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta 55281, Indonesia. sl.anwar@ugm.ac.id.
2
Institute of Pathology, Medizinische Hochschule Hannover, Hannover 30625, Germany. sl.anwar@ugm.ac.id.
3
PILAR (Philippine and Indonesian Scholar) Research and Education, 20 Station Road, Cambridge CB1 2JD, UK. sl.anwar@ugm.ac.id.
4
PILAR (Philippine and Indonesian Scholar) Research and Education, 20 Station Road, Cambridge CB1 2JD, UK. w.wulaningsih@ucl.ac.uk.
5
MRC (Medical Research Council) Unit for Lifelong Health and Ageing, University College London, London WC1B 5JU, UK. w.wulaningsih@ucl.ac.uk.
6
Division of Haematology/Oncology, Faculty of Medicine Universitas Gadjah Mada, Yogyakarta 55281, Indonesia. w.wulaningsih@ucl.ac.uk.
7
Institute of Pathology, Medizinische Hochschule Hannover, Hannover 30625, Germany. Lehmann.Ulrich@MH-Hannover.de.

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.

KEYWORDS:

cancer; epigenetics; genomic instability; non-coding RNAs; transposable elements

PMID:
28471386
PMCID:
PMC5454887
DOI:
10.3390/ijms18050974
[Indexed for MEDLINE]
Free PMC Article

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