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Telomerase antagonist imetelstat inhibits esophageal cancer cell growth and increases radiation-induced DNA breaks
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Radiology, Oncology and Radiation Science, Oncology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Radiology, Oncology and Radiation Science, Oncology.
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Medical Genetics. (hellström pigg)
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2012 (English)In: Biochimica et Biophysica Acta. Molecular Cell Research, ISSN 0167-4889, E-ISSN 1879-2596, Vol. 1823, no 12, 2130-2135 p.Article in journal (Refereed) Published
Abstract [en]

Telomerase is mainly active in human tumor cells, which provides an opportunity for a therapeutic window on telomerase targeting. We sought to evaluate the potential of the thio-phosphoramidate oligonucleotide inhibitor of telomerase, imetelstat, as a drug candidate for treatment of esophageal cancer. Our results showed that imetelstat inhibited telomerase activity in a dose-dependent manner in esophageal cancer cells. After only 1. week of imetelstat treatment, a reduction of colony formation ability of esophageal cancer cells was observed. Furthermore, long-term treatment with imetelstat decreased cell growth of esophageal cancer cells with different kinetics regarding telomere lengths. Short-term imetelstat treatment also increased γ-H2AX and 53BP1 foci staining in the esophageal cancer cell lines indicating a possible induction of DNA double strand breaks (DSBs). We also found that pre-treatment with imetelstat led to increased number and size of 53BP1 foci after ionizing radiation. The increase of 53BP1 foci number was especially pronounced during the first 1 h of repair whereas the increase of foci size was prominent later on. This study supports the potential of imetelstat as a therapeutic agent for the treatment of esophageal cancer.

Place, publisher, year, edition, pages
2012. Vol. 1823, no 12, 2130-2135 p.
Keyword [en]
γ-H2AX and 53BP1 foci, DNA double strand break, Esophageal cancer, Imetelstat, Telomerase
National Category
Medical and Health Sciences
Identifiers
URN: urn:nbn:se:uu:diva-184884DOI: 10.1016/j.bbamcr.2012.08.003ISI: 000312629200004OAI: oai:DiVA.org:uu-184884DiVA: diva2:570947
Available from: 2012-11-21 Created: 2012-11-15 Last updated: 2017-12-07Bibliographically approved

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Wu, XupingKarlsson, KristerSimonsson, MartinBergqvist, MichaelPaulsson-Karlsson, Ylva

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