Author: Viceconte N1, Dheur MS2, Majerova E1, Pierreux CE3, Baurain JF4, van Baren N5, Decottignies A6
Affiliation: <sup>1</sup>Genetic and Epigenetic Alterations of Genomes, de Duve Institute, Université catholique de Louvain, Brussels 1200, Belgium.
<sup>2</sup>Cellular Genetics, de Duve Institute, Université catholique de Louvain, Brussels 1200, Belgium.
<sup>3</sup>Cell Unit, de Duve Institute, Université catholique de Louvain, Brussels 1200, Belgium.
<sup>4</sup>Medical Oncology, Institut Roi Albert II, Cliniques universitaires Saint-Luc, Brussels 1200, Belgium.
<sup>5</sup>Cellular Genetics, de Duve Institute, Université catholique de Louvain, Brussels 1200, Belgium; Ludwig Institute for Cancer Research, Brussels 1200, Belgium.
<sup>6</sup>Genetic and Epigenetic Alterations of Genomes, de Duve Institute, Université catholique de Louvain, Brussels 1200, Belgium. Electronic address: anabelle.decottignies@uclouvain.be.
Conference/Journal: Cell Rep.
Date published: 2017 Jun 20
Other:
Volume ID: 19 , Issue ID: 12 , Pages: 2529-2543 , Special Notes: doi: 10.1016/j.celrep.2017.05.046. , Word Count: 142
Unlimited replicative potential is one of the hallmarks of cancer cells. In melanoma, hTERT (telomerase reverse transcriptase) is frequently overexpressed because of activating mutations in its promoter, suggesting that telomerase is necessary for melanoma development. We observed, however, that a subset of melanoma metastases and derived cell lines had no telomere maintenance mechanism. Early passages of the latter displayed long telomeres that progressively shortened and fused before cell death. We propose that, during melanoma formation, oncogenic mutations occur in precursor melanocytes with long telomeres, providing cells with sufficient replicative potential, thereby bypassing the need to re-activate telomerase. Our data further support the emerging idea that long telomeres promote melanoma formation. These observations are important when considering anticancer therapies targeting telomerase.
Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.
KEYWORDS: ever-shorter telomeres; immortalization; melanoma; telomerase; telomeres
PMID: 28636941 DOI: 10.1016/j.celrep.2017.05.046