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Anti-cancer binary system activated by bacteriophage HK022 integrase

The binary system presented in this work is based on the bacteriophage HK022 integrase recombinase that activates the expression of a silenced Diphtheria toxin gene, both controlled by the cancer specific hTERT promoter. Using a lung cancer mice model, assays of different apoptotic and anti-apoptoti...

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Detalles Bibliográficos
Autores principales: Elias, Amer, Gritsenko, Natasha, Gorovits, Rena, Spector, Itay, Prag, Gali, Yagil, Ezra, Kolot, Mikhail
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6007955/
https://www.ncbi.nlm.nih.gov/pubmed/29938000
http://dx.doi.org/10.18632/oncotarget.25512
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author Elias, Amer
Gritsenko, Natasha
Gorovits, Rena
Spector, Itay
Prag, Gali
Yagil, Ezra
Kolot, Mikhail
author_facet Elias, Amer
Gritsenko, Natasha
Gorovits, Rena
Spector, Itay
Prag, Gali
Yagil, Ezra
Kolot, Mikhail
author_sort Elias, Amer
collection PubMed
description The binary system presented in this work is based on the bacteriophage HK022 integrase recombinase that activates the expression of a silenced Diphtheria toxin gene, both controlled by the cancer specific hTERT promoter. Using a lung cancer mice model, assays of different apoptotic and anti-apoptotic factors have demonstrated that the Integrase based binary system is highly specific towards cancer cells and more efficient compared to the conventional mono system whose toxin is directly expressed under hTERT. In a mice survival test, this binary system demonstrated longer persistence compared to the untreated and the mono treated ones. The reason underlying the advantage of this binary system over the mono system seems to be an overexpression of various hTERT suppressing factors induced by the mono system.
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spelling pubmed-60079552018-06-22 Anti-cancer binary system activated by bacteriophage HK022 integrase Elias, Amer Gritsenko, Natasha Gorovits, Rena Spector, Itay Prag, Gali Yagil, Ezra Kolot, Mikhail Oncotarget Research Paper The binary system presented in this work is based on the bacteriophage HK022 integrase recombinase that activates the expression of a silenced Diphtheria toxin gene, both controlled by the cancer specific hTERT promoter. Using a lung cancer mice model, assays of different apoptotic and anti-apoptotic factors have demonstrated that the Integrase based binary system is highly specific towards cancer cells and more efficient compared to the conventional mono system whose toxin is directly expressed under hTERT. In a mice survival test, this binary system demonstrated longer persistence compared to the untreated and the mono treated ones. The reason underlying the advantage of this binary system over the mono system seems to be an overexpression of various hTERT suppressing factors induced by the mono system. Impact Journals LLC 2018-06-08 /pmc/articles/PMC6007955/ /pubmed/29938000 http://dx.doi.org/10.18632/oncotarget.25512 Text en Copyright: © 2018 Elias et al. http://creativecommons.org/licenses/by/3.0/ This article is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) (CC-BY), which permits unrestricted use and redistribution provided that the original author and source are credited.
spellingShingle Research Paper
Elias, Amer
Gritsenko, Natasha
Gorovits, Rena
Spector, Itay
Prag, Gali
Yagil, Ezra
Kolot, Mikhail
Anti-cancer binary system activated by bacteriophage HK022 integrase
title Anti-cancer binary system activated by bacteriophage HK022 integrase
title_full Anti-cancer binary system activated by bacteriophage HK022 integrase
title_fullStr Anti-cancer binary system activated by bacteriophage HK022 integrase
title_full_unstemmed Anti-cancer binary system activated by bacteriophage HK022 integrase
title_short Anti-cancer binary system activated by bacteriophage HK022 integrase
title_sort anti-cancer binary system activated by bacteriophage hk022 integrase
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6007955/
https://www.ncbi.nlm.nih.gov/pubmed/29938000
http://dx.doi.org/10.18632/oncotarget.25512
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