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...
Gespeichert in:
| Veröffentlicht in: | PloS one 2013-07, Vol.8 (7), p.e69485 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | |
|---|---|
| container_issue | 7 |
| container_start_page | e69485 |
| container_title | PloS one |
| container_volume | 8 |
| creator | Ma, Jia Zhang, Qing Chen, Sulian Fang, Binbin Yang, Qingling Chen, Changjie Miele, Lucio Sarkar, Fazlul H Xia, Jun Wang, Zhiwei |
| 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. |
| doi_str_mv | 10.1371/journal.pone.0069485 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_plos_</sourceid><recordid>TN_cdi_plos_journals_1440997225</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><doaj_id>oai_doaj_org_article_38d311fedd0844a5835cd50c7b6cfc25</doaj_id><sourcerecordid>3095102181</sourcerecordid><originalsourceid>FETCH-LOGICAL-c526t-5152c6109f42d24287bae38f61c789106123a1c53176a632125808cb0a38ffb93</originalsourceid><addsrcrecordid>eNp1ks1u1DAUhSMEoqXwBggssZ7BP7HjbJBQRelIRWxgbTnXTsajxB7sZNR5F16CF-kzNZmkVbtg5evrc79zZZ0se0_wmrCCfN6FIXrdrvfB2zXGoswlf5Gdk5LRlaCYvXxSn2VvUtphzJkU4nV2RllJaUHJefb3h-sDbIM30ekWmWOqBw-9Cx7tY-hCbxOqotWpR6A92IjAti3qXBP1SaW9Qc4fdJou_TaGodmi680VufuHNMDQDe0sPDg9CmFiWTPBzTD7hBqNzbE-WBRuj431KO0tOJveZq9q3Sb7bjkvst9X335dXq9ufn7fXH69WQGnol9xwikIgss6p4bmVBaVtkzWgkAhS4IFoUwT4IwUQgtGCeUSS6iwHkV1VbKL7OPM3bchqeVjkyJ5jsuyoJSPis2sMEHv1D66TsejCtqpUyPERunYO2itYtIwQmprDJZ5rrlkHAzHUFQCajixvixuQ9VZA9b3UbfPoM9fvNuqJhwUK6gQZTECPi2AGP4MNvX_WTmfVRBDStHWjw4EqylBD1NqSpBaEjSOfXi63ePQQ2TYPam3yPg</addsrcrecordid><sourcetype>Open Website</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1440997225</pqid></control><display><type>article</type><title>Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Free Full-Text Journals in Chemistry</source><source>Public Library of Science (PLoS)</source><creator>Ma, Jia ; Zhang, Qing ; Chen, Sulian ; Fang, Binbin ; Yang, Qingling ; Chen, Changjie ; Miele, Lucio ; Sarkar, Fazlul H ; Xia, Jun ; Wang, Zhiwei</creator><creatorcontrib>Ma, Jia ; Zhang, Qing ; Chen, Sulian ; Fang, Binbin ; Yang, Qingling ; Chen, Changjie ; Miele, Lucio ; Sarkar, Fazlul H ; Xia, Jun ; Wang, Zhiwei</creatorcontrib><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.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0069485</identifier><identifier>PMID: 23922721</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Accumulation ; Antioxidants ; Apoptosis ; Biochemistry ; Biology ; Blotting, Western ; Breast cancer ; Breast Neoplasms - genetics ; Breast Neoplasms - metabolism ; Cancer ; Catalase ; Cell adhesion & migration ; Cell cycle ; Cell Line, Tumor ; Cell migration ; Cell Movement - physiology ; Defects ; Deoxyribonucleic acid ; DNA ; Electron transport ; Electron transport chain ; Electrophoresis, Polyacrylamide Gel ; Female ; Gene expression ; Hematology ; Humans ; Hydrogen Peroxide - metabolism ; Hypoxia ; Hypoxia-inducible factor 1 ; Hypoxia-inducible factor 1a ; Invasiveness ; Medical research ; Medicine ; Mitochondria ; Mitochondria - metabolism ; Mitochondria - pathology ; Mitochondrial DNA ; Molecular biology ; Mutation ; NADH-ubiquinone oxidoreductase ; Oxidative stress ; Oxygen ; Penicillin ; Polyethylene glycol ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; Rotenone ; Species ; Studies ; Tumorigenesis ; Vascular endothelial growth factor ; Wound Healing - physiology</subject><ispartof>PloS one, 2013-07, Vol.8 (7), p.e69485</ispartof><rights>2013 Ma et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Ma et al 2013 Ma et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-5152c6109f42d24287bae38f61c789106123a1c53176a632125808cb0a38ffb93</citedby><cites>FETCH-LOGICAL-c526t-5152c6109f42d24287bae38f61c789106123a1c53176a632125808cb0a38ffb93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3726697/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3726697/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23922721$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Jia</creatorcontrib><creatorcontrib>Zhang, Qing</creatorcontrib><creatorcontrib>Chen, Sulian</creatorcontrib><creatorcontrib>Fang, Binbin</creatorcontrib><creatorcontrib>Yang, Qingling</creatorcontrib><creatorcontrib>Chen, Changjie</creatorcontrib><creatorcontrib>Miele, Lucio</creatorcontrib><creatorcontrib>Sarkar, Fazlul H</creatorcontrib><creatorcontrib>Xia, Jun</creatorcontrib><creatorcontrib>Wang, Zhiwei</creatorcontrib><title>Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species</title><title>PloS one</title><addtitle>PLoS One</addtitle><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.</description><subject>Accumulation</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Biochemistry</subject><subject>Biology</subject><subject>Blotting, Western</subject><subject>Breast cancer</subject><subject>Breast Neoplasms - genetics</subject><subject>Breast Neoplasms - metabolism</subject><subject>Cancer</subject><subject>Catalase</subject><subject>Cell adhesion & migration</subject><subject>Cell cycle</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement - physiology</subject><subject>Defects</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Electron transport</subject><subject>Electron transport chain</subject><subject>Electrophoresis, Polyacrylamide Gel</subject><subject>Female</subject><subject>Gene expression</subject><subject>Hematology</subject><subject>Humans</subject><subject>Hydrogen Peroxide - metabolism</subject><subject>Hypoxia</subject><subject>Hypoxia-inducible factor 1</subject><subject>Hypoxia-inducible factor 1a</subject><subject>Invasiveness</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Mitochondria</subject><subject>Mitochondria - metabolism</subject><subject>Mitochondria - pathology</subject><subject>Mitochondrial DNA</subject><subject>Molecular biology</subject><subject>Mutation</subject><subject>NADH-ubiquinone oxidoreductase</subject><subject>Oxidative stress</subject><subject>Oxygen</subject><subject>Penicillin</subject><subject>Polyethylene glycol</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Rotenone</subject><subject>Species</subject><subject>Studies</subject><subject>Tumorigenesis</subject><subject>Vascular endothelial growth factor</subject><subject>Wound Healing - physiology</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNp1ks1u1DAUhSMEoqXwBggssZ7BP7HjbJBQRelIRWxgbTnXTsajxB7sZNR5F16CF-kzNZmkVbtg5evrc79zZZ0se0_wmrCCfN6FIXrdrvfB2zXGoswlf5Gdk5LRlaCYvXxSn2VvUtphzJkU4nV2RllJaUHJefb3h-sDbIM30ekWmWOqBw-9Cx7tY-hCbxOqotWpR6A92IjAti3qXBP1SaW9Qc4fdJou_TaGodmi680VufuHNMDQDe0sPDg9CmFiWTPBzTD7hBqNzbE-WBRuj431KO0tOJveZq9q3Sb7bjkvst9X335dXq9ufn7fXH69WQGnol9xwikIgss6p4bmVBaVtkzWgkAhS4IFoUwT4IwUQgtGCeUSS6iwHkV1VbKL7OPM3bchqeVjkyJ5jsuyoJSPis2sMEHv1D66TsejCtqpUyPERunYO2itYtIwQmprDJZ5rrlkHAzHUFQCajixvixuQ9VZA9b3UbfPoM9fvNuqJhwUK6gQZTECPi2AGP4MNvX_WTmfVRBDStHWjw4EqylBD1NqSpBaEjSOfXi63ePQQ2TYPam3yPg</recordid><startdate>20130729</startdate><enddate>20130729</enddate><creator>Ma, Jia</creator><creator>Zhang, Qing</creator><creator>Chen, Sulian</creator><creator>Fang, Binbin</creator><creator>Yang, Qingling</creator><creator>Chen, Changjie</creator><creator>Miele, Lucio</creator><creator>Sarkar, Fazlul H</creator><creator>Xia, Jun</creator><creator>Wang, Zhiwei</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130729</creationdate><title>Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species</title><author>Ma, Jia ; Zhang, Qing ; Chen, Sulian ; Fang, Binbin ; Yang, Qingling ; Chen, Changjie ; Miele, Lucio ; Sarkar, Fazlul H ; Xia, Jun ; Wang, Zhiwei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-5152c6109f42d24287bae38f61c789106123a1c53176a632125808cb0a38ffb93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Accumulation</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Biochemistry</topic><topic>Biology</topic><topic>Blotting, Western</topic><topic>Breast cancer</topic><topic>Breast Neoplasms - genetics</topic><topic>Breast Neoplasms - metabolism</topic><topic>Cancer</topic><topic>Catalase</topic><topic>Cell adhesion & migration</topic><topic>Cell cycle</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement - physiology</topic><topic>Defects</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Electron transport</topic><topic>Electron transport chain</topic><topic>Electrophoresis, Polyacrylamide Gel</topic><topic>Female</topic><topic>Gene expression</topic><topic>Hematology</topic><topic>Humans</topic><topic>Hydrogen Peroxide - metabolism</topic><topic>Hypoxia</topic><topic>Hypoxia-inducible factor 1</topic><topic>Hypoxia-inducible factor 1a</topic><topic>Invasiveness</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Mitochondria</topic><topic>Mitochondria - metabolism</topic><topic>Mitochondria - pathology</topic><topic>Mitochondrial DNA</topic><topic>Molecular biology</topic><topic>Mutation</topic><topic>NADH-ubiquinone oxidoreductase</topic><topic>Oxidative stress</topic><topic>Oxygen</topic><topic>Penicillin</topic><topic>Polyethylene glycol</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>Rotenone</topic><topic>Species</topic><topic>Studies</topic><topic>Tumorigenesis</topic><topic>Vascular endothelial growth factor</topic><topic>Wound Healing - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Jia</creatorcontrib><creatorcontrib>Zhang, Qing</creatorcontrib><creatorcontrib>Chen, Sulian</creatorcontrib><creatorcontrib>Fang, Binbin</creatorcontrib><creatorcontrib>Yang, Qingling</creatorcontrib><creatorcontrib>Chen, Changjie</creatorcontrib><creatorcontrib>Miele, Lucio</creatorcontrib><creatorcontrib>Sarkar, Fazlul H</creatorcontrib><creatorcontrib>Xia, Jun</creatorcontrib><creatorcontrib>Wang, Zhiwei</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - Academic</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Agricultural Science Database</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biological Science Database</collection><collection>Engineering Database</collection><collection>Nursing & Allied Health Premium</collection><collection>Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Environmental Science Database</collection><collection>Materials Science Collection</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>Engineering Collection</collection><collection>Environmental Science Collection</collection><collection>Genetics Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Jia</au><au>Zhang, Qing</au><au>Chen, Sulian</au><au>Fang, Binbin</au><au>Yang, Qingling</au><au>Chen, Changjie</au><au>Miele, Lucio</au><au>Sarkar, Fazlul H</au><au>Xia, Jun</au><au>Wang, Zhiwei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-07-29</date><risdate>2013</risdate><volume>8</volume><issue>7</issue><spage>e69485</spage><pages>e69485-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>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.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23922721</pmid><doi>10.1371/journal.pone.0069485</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-07, Vol.8 (7), p.e69485 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1440997225 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
| subjects | Accumulation Antioxidants Apoptosis Biochemistry Biology Blotting, Western Breast cancer Breast Neoplasms - genetics Breast Neoplasms - metabolism Cancer Catalase Cell adhesion & migration Cell cycle Cell Line, Tumor Cell migration Cell Movement - physiology Defects Deoxyribonucleic acid DNA Electron transport Electron transport chain Electrophoresis, Polyacrylamide Gel Female Gene expression Hematology Humans Hydrogen Peroxide - metabolism Hypoxia Hypoxia-inducible factor 1 Hypoxia-inducible factor 1a Invasiveness Medical research Medicine Mitochondria Mitochondria - metabolism Mitochondria - pathology Mitochondrial DNA Molecular biology Mutation NADH-ubiquinone oxidoreductase Oxidative stress Oxygen Penicillin Polyethylene glycol Reactive oxygen species Reactive Oxygen Species - metabolism Rotenone Species Studies Tumorigenesis Vascular endothelial growth factor Wound Healing - physiology |
| title | Mitochondrial dysfunction promotes breast cancer cell migration and invasion through HIF1α accumulation via increased production of reactive oxygen species |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-09T20%3A28%3A37IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Mitochondrial%20dysfunction%20promotes%20breast%20cancer%20cell%20migration%20and%20invasion%20through%20HIF1%CE%B1%20accumulation%20via%20increased%20production%20of%20reactive%20oxygen%20species&rft.jtitle=PloS%20one&rft.au=Ma,%20Jia&rft.date=2013-07-29&rft.volume=8&rft.issue=7&rft.spage=e69485&rft.pages=e69485-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0069485&rft_dat=%3Cproquest_plos_%3E3095102181%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1440997225&rft_id=info:pmid/23922721&rft_doaj_id=oai_doaj_org_article_38d311fedd0844a5835cd50c7b6cfc25&rfr_iscdi=true |