Suppression of mitochondrial complex I influences cell metastatic properties
Despite the fact that mitochondrial dysfunction has an important role in tumorigenesis and metastasis, the underlying mechanism remains to be elucidated. Mitochondrial Complex I (NADH:ubiquinone oxidoreductase) is the first and the largest protein complex of the mitochondrial electron-transport chai...
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| creator | He, Xuelian Zhou, Aifen Lu, Hao Chen, Yong Huang, Guochang Yue, Xin Zhao, Peiwei Wu, Yanxiang |
| description | Despite the fact that mitochondrial dysfunction has an important role in tumorigenesis and metastasis, the underlying mechanism remains to be elucidated. Mitochondrial Complex I (NADH:ubiquinone oxidoreductase) is the first and the largest protein complex of the mitochondrial electron-transport chain (ETC),which has an essential role in maintaining mitochondrial function and integrity. In this study, we separately knocked down two subunits of mitochondrial complex I, GRIM-19 or NDUFS3, and investigated their effects on metastatic behaviors and explored the possible mechanisms. Our data showed that stable down-modulation of GRIM-19 or NDUFS3 decreased complex I activity and reactive oxygen species (ROS) production; led to enhanced cell adhesion, migration, invasion, and spheroid formation; and influenced the expressions of extracellular matrix (ECM) molecules and its related proteins. We also observed that the expressions of GRIM-19, NDUFS3, and ECM elements were correlated with invasive capabilities of breast cancer cell lines. These results suggest that inhibition of complex I affects metastatic properties of cancer cells, and mitochondrial ROS might play a crucial role in these processes by regulating ECM. |
| doi_str_mv | 10.1371/journal.pone.0061677 |
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Mitochondrial Complex I (NADH:ubiquinone oxidoreductase) is the first and the largest protein complex of the mitochondrial electron-transport chain (ETC),which has an essential role in maintaining mitochondrial function and integrity. In this study, we separately knocked down two subunits of mitochondrial complex I, GRIM-19 or NDUFS3, and investigated their effects on metastatic behaviors and explored the possible mechanisms. Our data showed that stable down-modulation of GRIM-19 or NDUFS3 decreased complex I activity and reactive oxygen species (ROS) production; led to enhanced cell adhesion, migration, invasion, and spheroid formation; and influenced the expressions of extracellular matrix (ECM) molecules and its related proteins. We also observed that the expressions of GRIM-19, NDUFS3, and ECM elements were correlated with invasive capabilities of breast cancer cell lines. These results suggest that inhibition of complex I affects metastatic properties of cancer cells, and mitochondrial ROS might play a crucial role in these processes by regulating ECM.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0061677</identifier><identifier>PMID: 23630608</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Antigens, CD - metabolism ; Apoptosis ; Apoptosis Regulatory Proteins - genetics ; Apoptosis Regulatory Proteins - metabolism ; Biology ; Breast cancer ; Cadherins - metabolism ; Cancer ; Cancer metastasis ; Cell adhesion ; Cell adhesion & migration ; Cell Adhesion Molecules - metabolism ; Cell Line, Tumor ; Cell migration ; Cell Movement ; Cell Proliferation ; Cell Shape ; Development and progression ; Electron transport ; Electron transport chain ; Electron Transport Complex I - genetics ; Electron Transport Complex I - metabolism ; Epithelial-Mesenchymal Transition ; Extracellular matrix ; Extracellular Matrix - metabolism ; Fibronectins - genetics ; Fibronectins - metabolism ; Gene Expression ; Gene Knockdown Techniques ; HeLa Cells ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Integrins - metabolism ; Invasiveness ; Laboratories ; Medical research ; Medicine ; Metastases ; Metastasis ; Mitochondria ; Mitochondria - enzymology ; Mitochondrial DNA ; Morphology ; NADH ; NADH Dehydrogenase - genetics ; NADH Dehydrogenase - metabolism ; NADH, NADPH Oxidoreductases - genetics ; NADH, NADPH Oxidoreductases - metabolism ; NADH-ubiquinone oxidoreductase ; Neoplasm Metastasis ; Nicotinamide adenine dinucleotide ; Oxidation ; Oxidoreductase ; Oxygen ; Phenotype ; Phosphorylation ; Proteins ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; RNA, Small Interfering - genetics ; Science ; Spheroids, Cellular ; Tumor cell lines ; Tumorigenesis ; Ubiquinone ; Ubiquinone oxidoreductase</subject><ispartof>PloS one, 2013-04, Vol.8 (4), p.e61677-e61677</ispartof><rights>COPYRIGHT 2013 Public Library of Science</rights><rights>2013 He 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 He et al 2013 He et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-c06a18290d8b002cca18da3251ee1016224a4459820fd1b04fd489c17e72cfe03</citedby><cites>FETCH-LOGICAL-c758t-c06a18290d8b002cca18da3251ee1016224a4459820fd1b04fd489c17e72cfe03</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/PMC3632579/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3632579/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23630608$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>He, Xuelian</creatorcontrib><creatorcontrib>Zhou, Aifen</creatorcontrib><creatorcontrib>Lu, Hao</creatorcontrib><creatorcontrib>Chen, Yong</creatorcontrib><creatorcontrib>Huang, Guochang</creatorcontrib><creatorcontrib>Yue, Xin</creatorcontrib><creatorcontrib>Zhao, Peiwei</creatorcontrib><creatorcontrib>Wu, Yanxiang</creatorcontrib><title>Suppression of mitochondrial complex I influences cell metastatic properties</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Despite the fact that mitochondrial dysfunction has an important role in tumorigenesis and metastasis, the underlying mechanism remains to be elucidated. Mitochondrial Complex I (NADH:ubiquinone oxidoreductase) is the first and the largest protein complex of the mitochondrial electron-transport chain (ETC),which has an essential role in maintaining mitochondrial function and integrity. In this study, we separately knocked down two subunits of mitochondrial complex I, GRIM-19 or NDUFS3, and investigated their effects on metastatic behaviors and explored the possible mechanisms. Our data showed that stable down-modulation of GRIM-19 or NDUFS3 decreased complex I activity and reactive oxygen species (ROS) production; led to enhanced cell adhesion, migration, invasion, and spheroid formation; and influenced the expressions of extracellular matrix (ECM) molecules and its related proteins. We also observed that the expressions of GRIM-19, NDUFS3, and ECM elements were correlated with invasive capabilities of breast cancer cell lines. These results suggest that inhibition of complex I affects metastatic properties of cancer cells, and mitochondrial ROS might play a crucial role in these processes by regulating ECM.</description><subject>Antigens, CD - metabolism</subject><subject>Apoptosis</subject><subject>Apoptosis Regulatory Proteins - genetics</subject><subject>Apoptosis Regulatory Proteins - metabolism</subject><subject>Biology</subject><subject>Breast cancer</subject><subject>Cadherins - metabolism</subject><subject>Cancer</subject><subject>Cancer metastasis</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell Adhesion Molecules - metabolism</subject><subject>Cell Line, Tumor</subject><subject>Cell migration</subject><subject>Cell Movement</subject><subject>Cell Proliferation</subject><subject>Cell Shape</subject><subject>Development and progression</subject><subject>Electron transport</subject><subject>Electron transport chain</subject><subject>Electron Transport Complex I - genetics</subject><subject>Electron Transport Complex I - metabolism</subject><subject>Epithelial-Mesenchymal Transition</subject><subject>Extracellular matrix</subject><subject>Extracellular Matrix - metabolism</subject><subject>Fibronectins - genetics</subject><subject>Fibronectins - metabolism</subject><subject>Gene Expression</subject><subject>Gene Knockdown Techniques</subject><subject>HeLa Cells</subject><subject>Humans</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>Integrins - metabolism</subject><subject>Invasiveness</subject><subject>Laboratories</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mitochondria</subject><subject>Mitochondria - enzymology</subject><subject>Mitochondrial DNA</subject><subject>Morphology</subject><subject>NADH</subject><subject>NADH Dehydrogenase - genetics</subject><subject>NADH Dehydrogenase - metabolism</subject><subject>NADH, NADPH Oxidoreductases - genetics</subject><subject>NADH, NADPH Oxidoreductases - metabolism</subject><subject>NADH-ubiquinone oxidoreductase</subject><subject>Neoplasm Metastasis</subject><subject>Nicotinamide adenine dinucleotide</subject><subject>Oxidation</subject><subject>Oxidoreductase</subject><subject>Oxygen</subject><subject>Phenotype</subject><subject>Phosphorylation</subject><subject>Proteins</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>RNA, Small Interfering - genetics</subject><subject>Science</subject><subject>Spheroids, Cellular</subject><subject>Tumor cell lines</subject><subject>Tumorigenesis</subject><subject>Ubiquinone</subject><subject>Ubiquinone oxidoreductase</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>eNqNkl2L1DAUhoso7of-A9GCsOjFjPlq0t4Iy-LHwMCCq96GTHo6kyFtukkq6783dbrLVPZCetEmfc57ct68WfYKoyWmAn_Yu8F3yi5718ESIY65EE-yU1xRsuAE0adH3yfZWQh7hApacv48OyGUU8RReZqtb4a-9xCCcV3umrw10emd62pvlM21a3sLd_kqN11jB-g0hFyDtXkLUYWootF5710PPhoIL7JnjbIBXk7v8-zH50_fr74u1tdfVleX64UWRRkXGnGFS1KhutwgRLROq1pRUmAAjDAnhCnGiqokqKnxBrGmZmWlsQBBdAOInmdvDrq9dUFORgSJKS3SVBUpErE6ELVTe9l70yr_Wzpl5N8N57dSpSNrC7JgKOlWhCFeMxCsUoAIZrpugHGCx24fp27DpoVaQxe9sjPR-Z_O7OTW_ZLJZFKIKgm8mwS8ux0gRNmaMLqoOnDDeG4mGE_NRvTtP-jj003UVqUB0tW41FePovKSiRILQhFN1PIRKj01tEan1DQm7c8K3s8KEhPhLm7VEIJc3Xz7f_b655y9OGJ3oGzcBWeHmDIX5iA7gNq7EDw0DyZjJMfQ37shx9DLKfSp7PXxBT0U3aec_gHu2_sk</recordid><startdate>20130422</startdate><enddate>20130422</enddate><creator>He, Xuelian</creator><creator>Zhou, Aifen</creator><creator>Lu, Hao</creator><creator>Chen, Yong</creator><creator>Huang, Guochang</creator><creator>Yue, Xin</creator><creator>Zhao, Peiwei</creator><creator>Wu, Yanxiang</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>IOV</scope><scope>ISR</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>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20130422</creationdate><title>Suppression of mitochondrial complex I influences cell metastatic properties</title><author>He, Xuelian ; Zhou, Aifen ; Lu, Hao ; Chen, Yong ; Huang, Guochang ; Yue, Xin ; Zhao, Peiwei ; Wu, Yanxiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-c06a18290d8b002cca18da3251ee1016224a4459820fd1b04fd489c17e72cfe03</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Antigens, CD - metabolism</topic><topic>Apoptosis</topic><topic>Apoptosis Regulatory Proteins - genetics</topic><topic>Apoptosis Regulatory Proteins - metabolism</topic><topic>Biology</topic><topic>Breast cancer</topic><topic>Cadherins - metabolism</topic><topic>Cancer</topic><topic>Cancer metastasis</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell Adhesion Molecules - metabolism</topic><topic>Cell Line, Tumor</topic><topic>Cell migration</topic><topic>Cell Movement</topic><topic>Cell Proliferation</topic><topic>Cell Shape</topic><topic>Development and progression</topic><topic>Electron transport</topic><topic>Electron transport chain</topic><topic>Electron Transport Complex I - genetics</topic><topic>Electron Transport Complex I - metabolism</topic><topic>Epithelial-Mesenchymal Transition</topic><topic>Extracellular matrix</topic><topic>Extracellular Matrix - metabolism</topic><topic>Fibronectins - genetics</topic><topic>Fibronectins - metabolism</topic><topic>Gene Expression</topic><topic>Gene Knockdown Techniques</topic><topic>HeLa Cells</topic><topic>Humans</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</topic><topic>Integrins - metabolism</topic><topic>Invasiveness</topic><topic>Laboratories</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Metastases</topic><topic>Metastasis</topic><topic>Mitochondria</topic><topic>Mitochondria - enzymology</topic><topic>Mitochondrial DNA</topic><topic>Morphology</topic><topic>NADH</topic><topic>NADH Dehydrogenase - genetics</topic><topic>NADH Dehydrogenase - metabolism</topic><topic>NADH, NADPH Oxidoreductases - genetics</topic><topic>NADH, NADPH Oxidoreductases - metabolism</topic><topic>NADH-ubiquinone oxidoreductase</topic><topic>Neoplasm Metastasis</topic><topic>Nicotinamide adenine dinucleotide</topic><topic>Oxidation</topic><topic>Oxidoreductase</topic><topic>Oxygen</topic><topic>Phenotype</topic><topic>Phosphorylation</topic><topic>Proteins</topic><topic>Reactive oxygen species</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>RNA, Small Interfering - genetics</topic><topic>Science</topic><topic>Spheroids, Cellular</topic><topic>Tumor cell lines</topic><topic>Tumorigenesis</topic><topic>Ubiquinone</topic><topic>Ubiquinone oxidoreductase</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>He, Xuelian</creatorcontrib><creatorcontrib>Zhou, Aifen</creatorcontrib><creatorcontrib>Lu, Hao</creatorcontrib><creatorcontrib>Chen, Yong</creatorcontrib><creatorcontrib>Huang, Guochang</creatorcontrib><creatorcontrib>Yue, Xin</creatorcontrib><creatorcontrib>Zhao, Peiwei</creatorcontrib><creatorcontrib>Wu, Yanxiang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</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 - 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Academic</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>He, Xuelian</au><au>Zhou, Aifen</au><au>Lu, Hao</au><au>Chen, Yong</au><au>Huang, Guochang</au><au>Yue, Xin</au><au>Zhao, Peiwei</au><au>Wu, Yanxiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Suppression of mitochondrial complex I influences cell metastatic properties</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-04-22</date><risdate>2013</risdate><volume>8</volume><issue>4</issue><spage>e61677</spage><epage>e61677</epage><pages>e61677-e61677</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Despite the fact that mitochondrial dysfunction has an important role in tumorigenesis and metastasis, the underlying mechanism remains to be elucidated. Mitochondrial Complex I (NADH:ubiquinone oxidoreductase) is the first and the largest protein complex of the mitochondrial electron-transport chain (ETC),which has an essential role in maintaining mitochondrial function and integrity. In this study, we separately knocked down two subunits of mitochondrial complex I, GRIM-19 or NDUFS3, and investigated their effects on metastatic behaviors and explored the possible mechanisms. Our data showed that stable down-modulation of GRIM-19 or NDUFS3 decreased complex I activity and reactive oxygen species (ROS) production; led to enhanced cell adhesion, migration, invasion, and spheroid formation; and influenced the expressions of extracellular matrix (ECM) molecules and its related proteins. We also observed that the expressions of GRIM-19, NDUFS3, and ECM elements were correlated with invasive capabilities of breast cancer cell lines. These results suggest that inhibition of complex I affects metastatic properties of cancer cells, and mitochondrial ROS might play a crucial role in these processes by regulating ECM.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>23630608</pmid><doi>10.1371/journal.pone.0061677</doi><tpages>e61677</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2013-04, Vol.8 (4), p.e61677-e61677 |
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| subjects | Antigens, CD - metabolism Apoptosis Apoptosis Regulatory Proteins - genetics Apoptosis Regulatory Proteins - metabolism Biology Breast cancer Cadherins - metabolism Cancer Cancer metastasis Cell adhesion Cell adhesion & migration Cell Adhesion Molecules - metabolism Cell Line, Tumor Cell migration Cell Movement Cell Proliferation Cell Shape Development and progression Electron transport Electron transport chain Electron Transport Complex I - genetics Electron Transport Complex I - metabolism Epithelial-Mesenchymal Transition Extracellular matrix Extracellular Matrix - metabolism Fibronectins - genetics Fibronectins - metabolism Gene Expression Gene Knockdown Techniques HeLa Cells Humans Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Integrins - metabolism Invasiveness Laboratories Medical research Medicine Metastases Metastasis Mitochondria Mitochondria - enzymology Mitochondrial DNA Morphology NADH NADH Dehydrogenase - genetics NADH Dehydrogenase - metabolism NADH, NADPH Oxidoreductases - genetics NADH, NADPH Oxidoreductases - metabolism NADH-ubiquinone oxidoreductase Neoplasm Metastasis Nicotinamide adenine dinucleotide Oxidation Oxidoreductase Oxygen Phenotype Phosphorylation Proteins Reactive oxygen species Reactive Oxygen Species - metabolism RNA, Small Interfering - genetics Science Spheroids, Cellular Tumor cell lines Tumorigenesis Ubiquinone Ubiquinone oxidoreductase |
| title | Suppression of mitochondrial complex I influences cell metastatic properties |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-16T05%3A32%3A52IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Suppression%20of%20mitochondrial%20complex%20I%20influences%20cell%20metastatic%20properties&rft.jtitle=PloS%20one&rft.au=He,%20Xuelian&rft.date=2013-04-22&rft.volume=8&rft.issue=4&rft.spage=e61677&rft.epage=e61677&rft.pages=e61677-e61677&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0061677&rft_dat=%3Cgale_plos_%3EA478172303%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1335060925&rft_id=info:pmid/23630608&rft_galeid=A478172303&rft_doaj_id=oai_doaj_org_article_540e7292406d4e749ae0214cdfe46210&rfr_iscdi=true |