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Carboxyl-terminal modulator protein induces apoptosis by regulating mitochondrial function in lung cancer cells

DC Field Value Language
dc.contributor.authorHwang, Soon-Kyung-
dc.contributor.authorMinai-Tehrani, Arash-
dc.contributor.authorYu, Kyeong-Nam-
dc.contributor.authorChang, Seung-Hee-
dc.contributor.authorKim, Ji-Eun-
dc.contributor.authorLee, Kee-Ho-
dc.contributor.authorPark, Jongsun-
dc.contributor.authorBeck, George R., Jr.-
dc.contributor.authorCho, Myung-Haing-
dc.date.accessioned2021-01-31T08:43:45Z-
dc.date.available2021-01-31T08:43:45Z-
dc.date.created2020-11-18-
dc.date.issued2012-05-
dc.identifier.citationInternational Journal of Oncology, Vol.40 No.5, pp.1515-1524-
dc.identifier.issn1019-6439-
dc.identifier.other116663-
dc.identifier.urihttps://hdl.handle.net/10371/172399-
dc.description.abstractSerine/threonine protein kinase 13 (PKB/Akt) is involved in cell survival and growth. Carboxyl-terminal modulator protein (CTMP), a novel Akt binding partner, prevents Akt activation at the plasma membrane in response to various stimuli, and thus possesses a tumor suppressor-like function. In a previous study, we have demonstrated that CTMP inhibits tumor progression by facilitating apoptosis in a mouse lung cancer model. However, the precise mechanism of CTMP-induced apoptosis remains to be elucidated. The present study was performed to examine the role of CTMP in mitochondrial-mediated apoptosis and regulation of mitochondrial function in human lung carcinoma cells. Our results showed that CTMP altered mitochondrial morphology and caused the release of cytochrome c by inhibiting OPA1 expression. Additionally, CTMP facilitated mitochondrial-mediated apoptosis by inhibiting heat-shock protein 27 and preventing cytochrome c interaction with Apaf-1. Our data suggest that CTMP may therefore play a critical role in mitochondrial-mediated apoptosis in lung cancer cells.-
dc.language영어-
dc.publisherDemetrios A. Spandidos Ed. & Pub.-
dc.titleCarboxyl-terminal modulator protein induces apoptosis by regulating mitochondrial function in lung cancer cells-
dc.typeArticle-
dc.contributor.AlternativeAuthor조명행-
dc.identifier.doi10.3892/ijo.2011.1319-
dc.citation.journaltitleInternational Journal of Oncology-
dc.identifier.wosid000302273400022-
dc.identifier.scopusid2-s2.0-84860298612-
dc.citation.endpage1524-
dc.citation.number5-
dc.citation.startpage1515-
dc.citation.volume40-
dc.identifier.sci000302273400022-
dc.description.isOpenAccessN-
dc.contributor.affiliatedAuthorCho, Myung-Haing-
dc.type.docTypeArticle-
dc.description.journalClass1-
dc.subject.keywordPlusCYTOCHROME-C-
dc.subject.keywordPlusOPA1-
dc.subject.keywordPlusDYNAMICS-
dc.subject.keywordPlusAKT-
dc.subject.keywordPlusPROLIFERATION-
dc.subject.keywordPlusMORPHOLOGY-
dc.subject.keywordPlusMEMBRANE-
dc.subject.keywordPlusPKB/AKT-
dc.subject.keywordPlusRELEASE-
dc.subject.keywordPlusPATHWAY-
dc.subject.keywordAuthorCTMP-
dc.subject.keywordAuthorapoptosis-
dc.subject.keywordAuthormitochondria-
dc.subject.keywordAuthorlung cancer cells-
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