Change search
ReferencesLink to record
Permanent link

Direct link
Telomerase antagonist imetelstat inhibits esophageal cancer cell growth and increases radiation-induced DNA breaks
Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
Show others and affiliations
2012 (English)In: Biochimica et Biophysica Acta. Molecular Cell Research, ISSN 0167-4889, 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 gamma-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
Elsevier, 2012. Vol. 1823, no 12, 2130-2135 p.
Keyword [en]
Telomerase, Esophageal cancer, Imetelstat, DNA double strand break, gamma-H2AX and 53BP1 foci
National Category
Cancer and Oncology
URN: urn:nbn:se:umu:diva-64453DOI: 10.1016/j.bbamcr.2012.08.003ISI: 000312629200004OAI: diva2:603274
Available from: 2013-02-05 Created: 2013-01-29 Last updated: 2013-02-05Bibliographically approved

Open Access in DiVA

No full text

Other links

Publisher's full text

Search in DiVA

By author/editor
Nordfjäll, Katarina
By organisation
In the same journal
Biochimica et Biophysica Acta. Molecular Cell Research
Cancer and Oncology

Search outside of DiVA

GoogleGoogle Scholar
The number of downloads is the sum of all downloads of full texts. It may include eg previous versions that are now no longer available

Altmetric score

Total: 24 hits
ReferencesLink to record
Permanent link

Direct link