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Telomerase antagoni...
Telomerase antagonist imetelstat inhibits esophageal cancer cell growth and increases radiation-induced DNA breaks
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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)
- Umeå universitet,Patologi
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- Karlsson, Krister (författare)
- Uppsala universitet,Medicinsk genetik,hellström pigg
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Qvarnström, Fredrik (författare)
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- Simonsson, Martin (författare)
- Uppsala universitet,Enheten för onkologi
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- Bergqvist, Michael (författare)
- Uppsala universitet,Enheten för onkologi
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Gryaznov, Sergei (författare)
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- Ekman, Simon (författare)
- Uppsala universitet,Enheten för onkologi
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- Paulsson-Karlsson, Ylva (författare)
- Uppsala universitet,Medicinsk genetik,hellström pigg
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(creator_code:org_t)
- Elsevier BV, 2012
- 2012
- Engelska.
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Ingår i: Biochimica et Biophysica Acta. Molecular Cell Research. - : Elsevier BV. - 0167-4889 .- 1879-2596. ; 1823:12, s. 2130-2135
- Relaterad länk:
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https://doi.org/10.1...
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https://urn.kb.se/re...
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https://doi.org/10.1...
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https://urn.kb.se/re...
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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 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.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Cancer och onkologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Cancer and Oncology (hsv//eng)
Nyckelord
- γ-H2AX and 53BP1 foci
- DNA double strand break
- Esophageal cancer
- Imetelstat
- Telomerase
Publikations- och innehållstyp
- ref (ämneskategori)
- art (ämneskategori)
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