Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species.
Although mitochondrial dysfunction has been observed in various types of human cancer cells, the molecular mechanism underlying mitochondrial dysfunction mediated tumorigenesis remains largely elusive. To further explore the function of mitochondria and their involvement in the pathogenic mechanisms...
| Main Authors: | , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2013-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3726697?pdf=render |
| _version_ | 1819052266587422720 |
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| author | Jia Ma Qing Zhang Sulian Chen Binbin Fang Qingling Yang Changjie Chen Lucio Miele Fazlul H Sarkar Jun Xia Zhiwei Wang |
| author_facet | Jia Ma Qing Zhang Sulian Chen Binbin Fang Qingling Yang Changjie Chen Lucio Miele Fazlul H Sarkar Jun Xia Zhiwei Wang |
| author_sort | Jia Ma |
| collection | DOAJ |
| description | Although mitochondrial dysfunction has been observed in various types of human cancer cells, the molecular mechanism underlying mitochondrial dysfunction mediated tumorigenesis remains largely elusive. To further explore the function of mitochondria and their involvement in the pathogenic mechanisms of cancer development, mitochondrial dysfunction clones of breast cancer cells were generated by rotenone treatment, a specific inhibitor of mitochondrial electron transport complex I. These clones were verified by mitochondrial respiratory defect measurement. Moreover, those clones exhibited increased reactive oxygen species (ROS), and showed higher migration and invasive behaviors compared with their parental cells. Furthermore, antioxidant N-acetyl cysteine, PEG-catalase, and mito-TEMPO effectively inhibited cell migration and invasion in these clones. Notably, ROS regulated malignant cellular behavior was in part mediated through upregulation of hypoxia-inducible factor-1 α and vascular endothelial growth factor. Our results suggest that mitochondrial dysfunction promotes cancer cell motility partly through HIF1α accumulation mediated via increased production of reactive oxygen species. |
| first_indexed | 2024-12-21T12:17:06Z |
| format | Article |
| id | doaj.art-38d311fedd0844a5835cd50c7b6cfc25 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-21T12:17:06Z |
| publishDate | 2013-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-38d311fedd0844a5835cd50c7b6cfc252022-12-21T19:04:25ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0187e6948510.1371/journal.pone.0069485Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species.Jia MaQing ZhangSulian ChenBinbin FangQingling YangChangjie ChenLucio MieleFazlul H SarkarJun XiaZhiwei WangAlthough mitochondrial dysfunction has been observed in various types of human cancer cells, the molecular mechanism underlying mitochondrial dysfunction mediated tumorigenesis remains largely elusive. To further explore the function of mitochondria and their involvement in the pathogenic mechanisms of cancer development, mitochondrial dysfunction clones of breast cancer cells were generated by rotenone treatment, a specific inhibitor of mitochondrial electron transport complex I. These clones were verified by mitochondrial respiratory defect measurement. Moreover, those clones exhibited increased reactive oxygen species (ROS), and showed higher migration and invasive behaviors compared with their parental cells. Furthermore, antioxidant N-acetyl cysteine, PEG-catalase, and mito-TEMPO effectively inhibited cell migration and invasion in these clones. Notably, ROS regulated malignant cellular behavior was in part mediated through upregulation of hypoxia-inducible factor-1 α and vascular endothelial growth factor. Our results suggest that mitochondrial dysfunction promotes cancer cell motility partly through HIF1α accumulation mediated via increased production of reactive oxygen species.http://europepmc.org/articles/PMC3726697?pdf=render |
| spellingShingle | Jia Ma Qing Zhang Sulian Chen Binbin Fang Qingling Yang Changjie Chen Lucio Miele Fazlul H Sarkar Jun Xia Zhiwei Wang Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species. PLoS ONE |
| title | Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species. |
| title_full | Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species. |
| title_fullStr | Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species. |
| title_full_unstemmed | Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species. |
| title_short | Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species. |
| title_sort | mitochondrial dysfunction promotes breast cancer cell migration and invasion through hif1α accumulation via increased production of reactive oxygen species |
| url | http://europepmc.org/articles/PMC3726697?pdf=render |
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