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Mitochondrial respiratory defects is linked with hepatoma cell invasiveness through claudin-1 induction

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dc.contributor.authorLee, Jong-Hyuk-
dc.contributor.authorKim, June-Hyung-
dc.contributor.authorYoon, Gyesoon-
dc.date.accessioned2012-06-11-
dc.date.available2012-06-11-
dc.identifier.urihttp://repository.ajou.ac.kr/handle/201003/6970-
dc.description.abstractClaudins are tight junction proteins that have recently been reported to be involved in cancer metastasis. Interestingly, we found that SNU human hepatoma cells with mitochondrial dysfunction have high level of Claudin-1(Cln-1) expression. In those HCC cells, Cln-1 played a key role in regulating invasiveness. Claudin-1 induction was also observed in human hepatocellular carcinoma tissues. Thus, we screened whether any specific mitochondrial defect was linked with Cln-1 induction. Among diverse respiratory inhibitors, complex I inhibition by rotenone most effectively induced Cln-1 expression at transcriptional level. This complex I defect-mediated Cln-1 induction was further confirmed by employing knockdown of NDUFA9, one of complex I subunits. These results suggest that mitochondrial respiratory defects are involved in cancer cell invasiveness through Cln-1 induction.-
dc.formatapplication/pdf-
dc.language.isoen-
dc.titleMitochondrial respiratory defects is linked with hepatoma cell invasiveness through claudin-1 inductionen
dc.typeOther-
dc.contributor.departmentDepartment of Biochemistry & Molecular Biology, Ajou University School of Medicine-
dc.type.localPoster-
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