Next Article in Journal
Letter to the Editor: Bioinformatics Analysis in Mice with Diet-Induced Nonalcoholic Steatohepatitis Treated with Astaxanthin and Vitamin E
Next Article in Special Issue
Epigenetic Bases of Aberrant Glycosylation in Cancer
Previous Article in Journal
Decrease of miR-195 Promotes Chondrocytes Proliferation and Maintenance of Chondrogenic Phenotype via Targeting FGF-18 Pathway
Previous Article in Special Issue
Histone H3 Acetyl K9 and Histone H3 Tri Methyl K4 as Prognostic Markers for Patients with Cervical Cancer
Article Menu
Issue 5 (May) cover image

Export Article

Open AccessReview
Int. J. Mol. Sci. 2017, 18(5), 974; doi:10.3390/ijms18050974

Transposable Elements in Human Cancer: Causes and Consequences of Deregulation

1
Division of Surgical Oncology, Department of Surgery Faculty of Medicine, Universitas Gadjah Mada, Yogyakarta 55281, Indonesia
2
Institute of Pathology, Medizinische Hochschule Hannover, Hannover 30625, Germany
3
PILAR (Philippine and Indonesian Scholar) Research and Education, 20 Station Road, Cambridge CB1 2JD, UK
4
MRC (Medical Research Council) Unit for Lifelong Health and Ageing, University College London, London WC1B 5JU, UK
5
Division of Haematology/Oncology, Faculty of Medicine Universitas Gadjah Mada, Yogyakarta 55281, Indonesia
*
Authors to whom correspondence should be addressed.
Academic Editor: Nicoletta Sacchi
Received: 21 March 2017 / Revised: 26 April 2017 / Accepted: 29 April 2017 / Published: 4 May 2017
(This article belongs to the Special Issue Cancer Epigenetics)
View Full-Text   |   Download PDF [1201 KB, uploaded 4 May 2017]   |  

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. View Full-Text
Keywords: transposable elements; epigenetics; cancer; genomic instability; non-coding RNAs transposable elements; epigenetics; cancer; genomic instability; non-coding RNAs
Figures

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Anwar, S.L.; Wulaningsih, W.; Lehmann, U. Transposable Elements in Human Cancer: Causes and Consequences of Deregulation. Int. J. Mol. Sci. 2017, 18, 974.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Int. J. Mol. Sci. EISSN 1422-0067 Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top