Apoptosis inhibitor 5 increases metastasis via Erk-mediated MMP expression

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dc.contributor.authorK H Song-
dc.contributor.authorSeok Ho Kim-
dc.contributor.authorKyung Hee Noh-
dc.contributor.authorH C Bae-
dc.contributor.authorJ H Kim-
dc.contributor.authorH J Lee-
dc.contributor.authorJinhoi Song-
dc.contributor.authorT H Kang-
dc.contributor.authorD W Kim-
dc.contributor.authorS J Oh-
dc.contributor.authorJ H Jeon-
dc.contributor.authorT W Kim-
dc.date.accessioned2017-04-19T10:08:58Z-
dc.date.available2017-04-19T10:08:58Z-
dc.date.issued2015-
dc.identifier.issn12258687-
dc.identifier.uri10.5483/BMBRep.2015.48.6.139ko
dc.identifier.urihttps://oak.kribb.re.kr/handle/201005/12744-
dc.description.abstractApoptosis inhibitor 5 (API5) has recently been identified as a tumor metastasis-regulating gene in cervical cancer cells. However, the precise mechanism of action for API5 is poorly understood. Here, we show that API5 increases the metastatic capacity of cervical cancer cells in vitro and in vivo via up-regulation of MMP-9. Interestingly, API5-mediated metastasis was strongly dependent on the Erk signaling pathway. Conversely, knock-down of API5 via siRNA technology decreased the level of phospho-Erk, the activity of the MMPs, in vitro invasion, and in vivo pulmonary metastasis. Moreover, the Erk-mediated metastatic action was abolished by the mutation of leucine into arginine within the heptad leucine repeat region, which affects protein-protein interactions. Thus, API5 increases the metastatic capacity of tumor cells by up-regulating MMP levels via activation of the Erk signaling pathway.-
dc.publisherSouth Korea-
dc.titleApoptosis inhibitor 5 increases metastasis via Erk-mediated MMP expression-
dc.title.alternativeApoptosis inhibitor 5 increases metastasis via Erk-mediated MMP expression-
dc.typeArticle-
dc.citation.titleBMB Reports-
dc.citation.number6-
dc.citation.endPage335-
dc.citation.startPage330-
dc.citation.volume48-
dc.contributor.affiliatedAuthorKyung Hee Noh-
dc.contributor.alternativeName송권호-
dc.contributor.alternativeName김석호-
dc.contributor.alternativeName노경희-
dc.contributor.alternativeName배현철-
dc.contributor.alternativeName김진희-
dc.contributor.alternativeName이효정-
dc.contributor.alternativeName송진회-
dc.contributor.alternativeName강태흥-
dc.contributor.alternativeName김동완-
dc.contributor.alternativeName오세진-
dc.contributor.alternativeName전주홍-
dc.contributor.alternativeName김태우-
dc.identifier.bibliographicCitationBMB Reports, vol. 48, no. 6, pp. 330-335-
dc.identifier.doi10.5483/BMBRep.2015.48.6.139-
dc.subject.keywordApoptosis inhibitor 5-
dc.subject.keywordCervical cancer-
dc.subject.keywordMatrix metaloproteinase-
dc.subject.keywordMetastasis-
dc.subject.localApoptosis inhibitor 5-
dc.subject.localCervical cancer-
dc.subject.localMatrix metaloproteinase-
dc.subject.localMetastasis-
dc.description.journalClassY-
Appears in Collections:
Division of Research on National Challenges > Stem Cell Convergenece Research Center > 1. Journal Articles
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