Hypoxia-inducible factor HIF-1? modulates drugs resistance in colon cancer cells
Introduction: Drug resistance mechanisms may be associated with decreased cell death and its induction may depend on the response to oxidative stress caused by hypoxia. The correlation between hypoxia-inducible factor HIF-1?, the number of reactive oxygen species and their effect on cell survival ha...
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Universidad Nacional de Colombia
2018
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Acceso en línea: | https://repository.urosario.edu.co/handle/10336/23196 https://doi.org/10.15446/revfacmed.v66n4.55149 |
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ir-10336-231962022-05-02T12:37:16Z Hypoxia-inducible factor HIF-1? modulates drugs resistance in colon cancer cells Factor inducible por hipoxia HIF-1? modula la resistencia a drogas en células de cáncer de colon Pinzón-Daza M.L. Cuellar Y. Ondo-Méndez, Alejandro Matheus, Luisa Del Riesgo Prendes, Lilia Castillo F. Garzón R. Apoptosis Cell hypoxia Colon cancer Doxorubicin (mesh) Introduction: Drug resistance mechanisms may be associated with decreased cell death and its induction may depend on the response to oxidative stress caused by hypoxia. The correlation between hypoxia-inducible factor HIF-1?, the number of reactive oxygen species and their effect on cell survival has not yet been evaluated. Objective: The purpose of this study was to evaluate the effect of HIF-1? activity and reactive oxygen species (ROS) accumulation in apoptosis of colon cancer cells. Materials and methods: HT29 colon cancer cells were treated with Cobalt(II) chloride (CoCl2) or doxorubicin and the activity of HIF-1? was determined by ELISA assay. ROS were determined using fluorescence probe carboxy-H2DFFDA. Apoptosis was assessed by caspase-3 activation analysis, and PUMA and BAX mRNA levels by qRT-PCR. The reduction of the antiapoptotic effect due to hypoxia was attenuated by use of the endonuclease APE-1 (E3330) inhibitor. The endonuclease E3330 APE-1 inhibitor allowed evaluating the effect of ROS generated by doxorubicin and CoCl2 on apoptosis. Results: Chemical hypoxia in combination with doxorubicin is an oxidative stressor in HT29 cells and induces a reduction in the apoptotic process in a time-dependent manner. Conclusion: Resistance to hypoxia and doxorubicin-mediated cell death could be controlled by a mechanism related to the activity of HIF-1? and the amount of reactive oxygen species generated. © 2018, Universidad Nacional de Colombia. All rights reserved. 2018 2020-05-26T00:00:18Z info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion https://repository.urosario.edu.co/handle/10336/23196 https://doi.org/10.15446/revfacmed.v66n4.55149 eng info:eu-repo/semantics/openAccess application/pdf Universidad Nacional de Colombia instname:Universidad del Rosario |
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EdocUR - Universidad del Rosario |
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language |
Inglés (English) |
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Apoptosis Cell hypoxia Colon cancer Doxorubicin (mesh) |
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Apoptosis Cell hypoxia Colon cancer Doxorubicin (mesh) Pinzón-Daza M.L. Cuellar Y. Ondo-Méndez, Alejandro Matheus, Luisa Del Riesgo Prendes, Lilia Castillo F. Garzón R. Hypoxia-inducible factor HIF-1? modulates drugs resistance in colon cancer cells |
description |
Introduction: Drug resistance mechanisms may be associated with decreased cell death and its induction may depend on the response to oxidative stress caused by hypoxia. The correlation between hypoxia-inducible factor HIF-1?, the number of reactive oxygen species and their effect on cell survival has not yet been evaluated. Objective: The purpose of this study was to evaluate the effect of HIF-1? activity and reactive oxygen species (ROS) accumulation in apoptosis of colon cancer cells. Materials and methods: HT29 colon cancer cells were treated with Cobalt(II) chloride (CoCl2) or doxorubicin and the activity of HIF-1? was determined by ELISA assay. ROS were determined using fluorescence probe carboxy-H2DFFDA. Apoptosis was assessed by caspase-3 activation analysis, and PUMA and BAX mRNA levels by qRT-PCR. The reduction of the antiapoptotic effect due to hypoxia was attenuated by use of the endonuclease APE-1 (E3330) inhibitor. The endonuclease E3330 APE-1 inhibitor allowed evaluating the effect of ROS generated by doxorubicin and CoCl2 on apoptosis. Results: Chemical hypoxia in combination with doxorubicin is an oxidative stressor in HT29 cells and induces a reduction in the apoptotic process in a time-dependent manner. Conclusion: Resistance to hypoxia and doxorubicin-mediated cell death could be controlled by a mechanism related to the activity of HIF-1? and the amount of reactive oxygen species generated. © 2018, Universidad Nacional de Colombia. All rights reserved. |
format |
Artículo (Article) |
author |
Pinzón-Daza M.L. Cuellar Y. Ondo-Méndez, Alejandro Matheus, Luisa Del Riesgo Prendes, Lilia Castillo F. Garzón R. |
author_facet |
Pinzón-Daza M.L. Cuellar Y. Ondo-Méndez, Alejandro Matheus, Luisa Del Riesgo Prendes, Lilia Castillo F. Garzón R. |
author_sort |
Pinzón-Daza M.L. |
title |
Hypoxia-inducible factor HIF-1? modulates drugs resistance in colon cancer cells |
title_short |
Hypoxia-inducible factor HIF-1? modulates drugs resistance in colon cancer cells |
title_full |
Hypoxia-inducible factor HIF-1? modulates drugs resistance in colon cancer cells |
title_fullStr |
Hypoxia-inducible factor HIF-1? modulates drugs resistance in colon cancer cells |
title_full_unstemmed |
Hypoxia-inducible factor HIF-1? modulates drugs resistance in colon cancer cells |
title_sort |
hypoxia-inducible factor hif-1? modulates drugs resistance in colon cancer cells |
publisher |
Universidad Nacional de Colombia |
publishDate |
2018 |
url |
https://repository.urosario.edu.co/handle/10336/23196 https://doi.org/10.15446/revfacmed.v66n4.55149 |
_version_ |
1740172523318804480 |
score |
12,131701 |