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The Protective Roles of ROS-Mediated Mitophagy on (125)I Seeds Radiation Induced Cell Death in HCT116 Cells
For many unresectable carcinomas and locally recurrent cancers (LRC), (125)I seeds brachytherapy is a feasible, effective, and safe treatment. Several studies have shown that (125)I seeds radiation exerts anticancer activity by triggering DNA damage. However, recent evidence shows mitochondrial qual...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5227180/ https://www.ncbi.nlm.nih.gov/pubmed/28119765 http://dx.doi.org/10.1155/2016/9460462 |
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author | Hu, Lelin Wang, Hao Huang, Li Zhao, Yong Wang, Junjie |
author_facet | Hu, Lelin Wang, Hao Huang, Li Zhao, Yong Wang, Junjie |
author_sort | Hu, Lelin |
collection | PubMed |
description | For many unresectable carcinomas and locally recurrent cancers (LRC), (125)I seeds brachytherapy is a feasible, effective, and safe treatment. Several studies have shown that (125)I seeds radiation exerts anticancer activity by triggering DNA damage. However, recent evidence shows mitochondrial quality to be another crucial determinant of cell fate, with mitophagy playing a central role in this control mechanism. Herein, we found that (125)I seeds irradiation injured mitochondria, leading to significantly elevated mitochondrial and intracellular ROS (reactive oxygen species) levels in HCT116 cells. The accumulation of mitochondrial ROS increased the expression of HIF-1α and its target genes BINP3 and NIX (BINP3L), which subsequently triggered mitophagy. Importantly, (125)I seeds radiation induced mitophagy promoted cells survival and protected HCT116 cells from apoptosis. These results collectively indicated that (125)I seeds radiation triggered mitophagy by upregulating the level of ROS to promote cellular homeostasis and survival. The present study uncovered the critical role of mitophagy in modulating the sensitivity of tumor cells to radiation therapy and suggested that chemotherapy targeting on mitophagy might improve the efficiency of (125)I seeds radiation treatment, which might be of clinical significance in tumor therapy. |
format | Online Article Text |
id | pubmed-5227180 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-52271802017-01-24 The Protective Roles of ROS-Mediated Mitophagy on (125)I Seeds Radiation Induced Cell Death in HCT116 Cells Hu, Lelin Wang, Hao Huang, Li Zhao, Yong Wang, Junjie Oxid Med Cell Longev Research Article For many unresectable carcinomas and locally recurrent cancers (LRC), (125)I seeds brachytherapy is a feasible, effective, and safe treatment. Several studies have shown that (125)I seeds radiation exerts anticancer activity by triggering DNA damage. However, recent evidence shows mitochondrial quality to be another crucial determinant of cell fate, with mitophagy playing a central role in this control mechanism. Herein, we found that (125)I seeds irradiation injured mitochondria, leading to significantly elevated mitochondrial and intracellular ROS (reactive oxygen species) levels in HCT116 cells. The accumulation of mitochondrial ROS increased the expression of HIF-1α and its target genes BINP3 and NIX (BINP3L), which subsequently triggered mitophagy. Importantly, (125)I seeds radiation induced mitophagy promoted cells survival and protected HCT116 cells from apoptosis. These results collectively indicated that (125)I seeds radiation triggered mitophagy by upregulating the level of ROS to promote cellular homeostasis and survival. The present study uncovered the critical role of mitophagy in modulating the sensitivity of tumor cells to radiation therapy and suggested that chemotherapy targeting on mitophagy might improve the efficiency of (125)I seeds radiation treatment, which might be of clinical significance in tumor therapy. Hindawi Publishing Corporation 2016 2016-12-29 /pmc/articles/PMC5227180/ /pubmed/28119765 http://dx.doi.org/10.1155/2016/9460462 Text en |
spellingShingle | Research Article Hu, Lelin Wang, Hao Huang, Li Zhao, Yong Wang, Junjie The Protective Roles of ROS-Mediated Mitophagy on (125)I Seeds Radiation Induced Cell Death in HCT116 Cells |
title | The Protective Roles of ROS-Mediated Mitophagy on (125)I Seeds Radiation Induced Cell Death in HCT116 Cells |
title_full | The Protective Roles of ROS-Mediated Mitophagy on (125)I Seeds Radiation Induced Cell Death in HCT116 Cells |
title_fullStr | The Protective Roles of ROS-Mediated Mitophagy on (125)I Seeds Radiation Induced Cell Death in HCT116 Cells |
title_full_unstemmed | The Protective Roles of ROS-Mediated Mitophagy on (125)I Seeds Radiation Induced Cell Death in HCT116 Cells |
title_short | The Protective Roles of ROS-Mediated Mitophagy on (125)I Seeds Radiation Induced Cell Death in HCT116 Cells |
title_sort | protective roles of ros-mediated mitophagy on (125)i seeds radiation induced cell death in hct116 cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5227180/ https://www.ncbi.nlm.nih.gov/pubmed/28119765 http://dx.doi.org/10.1155/2016/9460462 |
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