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The effect of the t...
The effect of the telomerase antagonist Imetelstat in esophageal carcinoma
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- wu, xuping (författare)
- Uppsala universitet,Enheten för onkologi
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- Smavadati, Shirin (författare)
- Uppsala universitet,Enheten för onkologi
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- Nordfjäll, Katarina (författare)
- Department of Medical Biosciences, pathology, Umeå University
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visa fler...
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- Karlsson, Krister (författare)
- Uppsala universitet,Institutionen för immunologi, genetik och patologi
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- Qvarnström, Fredrik (författare)
- Uppsala universitet,Enheten för onkologi
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- Simonsson, Martin (författare)
- Uppsala universitet,Enheten för onkologi
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- Bergquist, Michael (författare)
- Uppsala universitet,Enheten för onkologi
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- Gryaznov, Sergei (författare)
- Geron Corporation, Menlo Park, CA, USA
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- Ekman, Simon (författare)
- Uppsala universitet,Enheten för onkologi
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- Paulsson-Karlsson, Ylva (författare)
- Uppsala universitet,Institutionen för immunologi, genetik och patologi
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visa färre...
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(creator_code:org_t)
- Engelska.
- Relaterad länk:
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https://urn.kb.se/re...
Abstract
Ämnesord
Stäng
- 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 one 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. Cell cycle analysis demonstrated that short-term treatment with Imetelstat resulted in increased percentage of cells in G1 phase. 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.
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