Full metadata record
DC Field | Value | Language |
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dc.contributor.author | 이공주 | - |
dc.date.accessioned | 2016-08-27T04:08:52Z | - |
dc.date.available | 2016-08-27T04:08:52Z | - |
dc.date.issued | 2015 | - |
dc.identifier.issn | 1949-2553 | - |
dc.identifier.other | OAK-15365 | - |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/217441 | - |
dc.description.abstract | This study explored the role of ubiquitin C-terminal hydrolase-L1 (UCH-L1) in the production of ROS and tumor invasion. UCH-L1 was found to increase cellular ROS levels and promote cell invasion. Silencing UCH-L1, as well as inhibition of H2O2 generation by catalase or by DPI, a NOX inhibitor, suppressed the migration potential of B16F10 cells, indicating that UCH-L1 promotes cell migration by up-regulating H2O2 generation. Silencing NOX4, which generates H2O2, with siRNA eliminated the effect of UCH-L1 on cell migration. On the other hand, NOX4 overexpressed in HeLa cells happens to be ubiquitinated, and NOX4 following deubiquitination by UCH-L1, restored H2O2 -generating activity. These in vitro findings are consistent with the results obtained in vivo with catalase (-/-) C57BL/6J mice. When H2O2 and UCH-L1 levels were independently varied in these animals, the former by infecting with H2O2 -scavenging adenovirus-catalase, and the latter by overexpressing or silencing UCH-L1, pulmonary metastasis of B16F10 cells overexpressing UCH-L1 increased significantly in catalase (-/-) mice. In contrast, invasion did not increase when UCH-L1 was silenced in the B16F10 cells. These findings indicate that H2O2 levels regulated by UCH-L1 are necessary for cell invasion to occur and demonstrate that UCH-L1 promotes cell invasion by up-regulating H2O2 via deubiquitination of NOX4. | - |
dc.language | English | - |
dc.publisher | IMPACT JOURNALS LLC | - |
dc.subject | UCH-L1 | - |
dc.subject | ubiquitination | - |
dc.subject | hydrogen peroxide | - |
dc.subject | NOX4 | - |
dc.subject | invasion | - |
dc.title | Ubiquitin C-terminal hydrolase-L1 increases cancer cell invasion by modulating hydrogen peroxide generated via NADPH oxidase 4 | - |
dc.type | Article | - |
dc.relation.issue | 18 | - |
dc.relation.volume | 6 | - |
dc.relation.index | SCIE | - |
dc.relation.index | SCOPUS | - |
dc.relation.startpage | 16287 | - |
dc.relation.lastpage | 16303 | - |
dc.relation.journaltitle | ONCOTARGET | - |
dc.identifier.wosid | WOS:000359012000061 | - |
dc.identifier.scopusid | 2-s2.0-84937942455 | - |
dc.author.google | Kim, Hyun Jung | - |
dc.author.google | Magesh, Venkataraman | - |
dc.author.google | Lee, Jae-Jin | - |
dc.author.google | Kim, Sun | - |
dc.author.google | Knaus, Ulla G. | - |
dc.author.google | Lee, Kong-Joo | - |
dc.contributor.scopusid | 이공주(7501497635;57191532162) | - |
dc.date.modifydate | 20230208115507 | - |