Enhanced radiation response in radioresistant MCF-7 cells by targeting peroxiredoxin II

Anthony Joseph Gomez Diaz,1 Daniel Tamae,2 Yun Yen,3 JianJian Li,4 Tieli Wang1 1Department of Chemistry and Biochemistry, California State University at Dominguez Hills, Carson, CA, 2Center of Excellence in Environmental Toxicology, Department of Pharmacology, University of Pennsylvania, Philadelphi...

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Autores principales: Diaz AJG, Tamae D, Yen Y, Li JJ, Wang T
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Publicado: Dove Medical Press 2013
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spelling oai:doaj.org-article:05c9fc74c0a941fe852f8c3efdfa88d42021-12-02T06:48:14ZEnhanced radiation response in radioresistant MCF-7 cells by targeting peroxiredoxin II1179-1314https://doaj.org/article/05c9fc74c0a941fe852f8c3efdfa88d42013-10-01T00:00:00Zhttp://www.dovepress.com/enhanced-radiation-response-in-radioresistant-mcf-7-cells-by-targeting-a14670https://doaj.org/toc/1179-1314Anthony Joseph Gomez Diaz,1 Daniel Tamae,2 Yun Yen,3 JianJian Li,4 Tieli Wang1 1Department of Chemistry and Biochemistry, California State University at Dominguez Hills, Carson, CA, 2Center of Excellence in Environmental Toxicology, Department of Pharmacology, University of Pennsylvania, Philadelphia, PA, 3Department of Clinical and Molecular Pharmacology, Beckman Research Institute of City of Hope National Medical Center, Duarte, CA, 4Department of Radiation Oncology, University of California Davis, Sacramento, CA, USA Abstract: In our previous study, we identified that a protein target, peroxiredoxin II (PrxII), is overexpressed in radioresistant MCF+FIR3 breast-cancer cells and found that its expression and function is associated with breast-cancer radiation sensitivity or resistance. Small interference RNA (siRNA) targeting PrxII gene expression was able to sensitize MCF+FIR3 radioresistant breast-cancer cells to ionizing radiation. The major focus of this work was to investigate how the radiation response of MCF+FIR3 radioresistant cells was affected by the siRNA that inhibits PrxII gene expression. Our results, presented here, show that silencing PrxII gene expression increased cellular toxicity by altering cellular thiol status, inhibiting Ca2+ efflux from the cells, and perturbing the intracellular Ca2+ homeostasis. By combining radiotherapy and siRNA technology, we hope to develop new therapeutic strategies that may have potential to enhance the efficacy of chemotherapeutic agents due to this technology's property of targeting to specific cancer-related genes. Keywords: siRNA, PrxII, radiation resistance, Ca2+, MCF+FIR3Diaz AJGTamae DYen YLi JJWang TDove Medical PressarticleNeoplasms. Tumors. Oncology. Including cancer and carcinogensRC254-282ENBreast Cancer: Targets and Therapy, Vol 2013, Iss default, Pp 87-101 (2013)
institution DOAJ
collection DOAJ
language EN
topic Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
spellingShingle Neoplasms. Tumors. Oncology. Including cancer and carcinogens
RC254-282
Diaz AJG
Tamae D
Yen Y
Li JJ
Wang T
Enhanced radiation response in radioresistant MCF-7 cells by targeting peroxiredoxin II
description Anthony Joseph Gomez Diaz,1 Daniel Tamae,2 Yun Yen,3 JianJian Li,4 Tieli Wang1 1Department of Chemistry and Biochemistry, California State University at Dominguez Hills, Carson, CA, 2Center of Excellence in Environmental Toxicology, Department of Pharmacology, University of Pennsylvania, Philadelphia, PA, 3Department of Clinical and Molecular Pharmacology, Beckman Research Institute of City of Hope National Medical Center, Duarte, CA, 4Department of Radiation Oncology, University of California Davis, Sacramento, CA, USA Abstract: In our previous study, we identified that a protein target, peroxiredoxin II (PrxII), is overexpressed in radioresistant MCF+FIR3 breast-cancer cells and found that its expression and function is associated with breast-cancer radiation sensitivity or resistance. Small interference RNA (siRNA) targeting PrxII gene expression was able to sensitize MCF+FIR3 radioresistant breast-cancer cells to ionizing radiation. The major focus of this work was to investigate how the radiation response of MCF+FIR3 radioresistant cells was affected by the siRNA that inhibits PrxII gene expression. Our results, presented here, show that silencing PrxII gene expression increased cellular toxicity by altering cellular thiol status, inhibiting Ca2+ efflux from the cells, and perturbing the intracellular Ca2+ homeostasis. By combining radiotherapy and siRNA technology, we hope to develop new therapeutic strategies that may have potential to enhance the efficacy of chemotherapeutic agents due to this technology's property of targeting to specific cancer-related genes. Keywords: siRNA, PrxII, radiation resistance, Ca2+, MCF+FIR3
format article
author Diaz AJG
Tamae D
Yen Y
Li JJ
Wang T
author_facet Diaz AJG
Tamae D
Yen Y
Li JJ
Wang T
author_sort Diaz AJG
title Enhanced radiation response in radioresistant MCF-7 cells by targeting peroxiredoxin II
title_short Enhanced radiation response in radioresistant MCF-7 cells by targeting peroxiredoxin II
title_full Enhanced radiation response in radioresistant MCF-7 cells by targeting peroxiredoxin II
title_fullStr Enhanced radiation response in radioresistant MCF-7 cells by targeting peroxiredoxin II
title_full_unstemmed Enhanced radiation response in radioresistant MCF-7 cells by targeting peroxiredoxin II
title_sort enhanced radiation response in radioresistant mcf-7 cells by targeting peroxiredoxin ii
publisher Dove Medical Press
publishDate 2013
url https://doaj.org/article/05c9fc74c0a941fe852f8c3efdfa88d4
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AT tamaed enhancedradiationresponseinradioresistantmcf7cellsbytargetingperoxiredoxinii
AT yeny enhancedradiationresponseinradioresistantmcf7cellsbytargetingperoxiredoxinii
AT lijj enhancedradiationresponseinradioresistantmcf7cellsbytargetingperoxiredoxinii
AT wangt enhancedradiationresponseinradioresistantmcf7cellsbytargetingperoxiredoxinii
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