Cancer Research AACR Conference on Molecular Diagnostics - 2008 AACR Conference on Molecular Diagnostics - 2008
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[Cancer Research 63, 6149-6153, October 1, 2003]
© 2003 American Association for Cancer Research

Advances in Brief

Resistance to Senescence Induction and Telomere Shortening by a G-Quadruplex Ligand Inhibitor of Telomerase1

Dennis Gomez, Nassera Aouali, Alexandra Renaud, Céline Douarre, Kazuo Shin-ya, Jamal Tazi, Sophie Martinez, Chantal Trentesaux, Hamid Morjani and Jean-François Riou2

Onco-Pharmacologie [D. G., C. D., C. T., J-F. R.], Unité Mixte de Recherche (UMR) 6142 Centre National de la Recherche Scientifique (CNRS) [N. A., A. R., C. D., C. T., H. M.], and Equipe d’Accueil 2070 [S. M.], Institut Fédératif de Recherche 53, Unité de Formation et de Recherche de Pharmacie, Université de Reims Champagne-Ardenne, 51096 Reims Cedex, France; Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo 113-0032, Japan [K. S.]; and Institut de Génétique Moléculaire, UMR 5535 CNRS, IFR 122, 34293 Montpellier cedex, France [J. T.]

The molecular mechanisms induced by G-quadruplex ligands to trigger senescence in mammalian cells are still unknown, although the critical role of telomerase is highly suspected. JFA2 cells selected for resistance to senescence induced by the G-quadruplex ligand 12459 presented an overexpression of hTERT transcript that correlated to a functional increase in telomerase activity and telomere length. Consistently, treatment with 12459 failed to trigger senescence and telomere shortening in JFA2 cells. Resistant cells also presented cross-resistance for senescence induction to telomestatin, another G-quadruplex ligand from a different series, but not to other anticancer agents, indicating the selectivity of the resistance mechanism. We, thus, provide evidence that telomerase activity and telomere length are key cellular determinants of the resistance to G-quadruplex ligands.




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