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Akt regulation of Aven contributes to the sensitivity of cancer cells to chemotherapeutic agents

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dc.contributor.authorHan, Kyoung-Youn-
dc.contributor.authorHwang, Jee Won-
dc.contributor.authorBae, Gyu-Un-
dc.contributor.authorKim, Su-Nam-
dc.contributor.authorKim, Yong Kee-
dc.date.available2021-02-22T11:35:42Z-
dc.date.issued2015-05-
dc.identifier.issn1791-2997-
dc.identifier.issn1791-3004-
dc.identifier.urihttps://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/10542-
dc.description.abstractIn the present study, it was demonstrated that the protein level of the apoptosis inhibitor Aven is regulated by the Akt signaling pathway, evidenced by the observation that Aven levels were significantly increased in MCF7 constitutively active (CA)-Akt cells and significantly inhibited following treatment with LY294002. This increase in Aven appears not to be mediated by transcriptional regulation and protein stabilization. However, the level of Aven was inversely correlated with the level of cathepsin D, which is a protease responsible for generating the C-terminal of Aven, Delta N-Aven, indicating that the level of Aven appears to be regulated by cathepsin D activity. It has previously been reported that Delta N-Aven is the active form of Aven, which functions as an anti-apoptotic molecule. Notably, low levels of Delta N-Aven were detected in MCF7 CA-Akt cells, which were more sensitive to anticancer drugs. Taken together, the current results suggest that the expression of Aven is regulated by the Akt signaling pathway through cathepsin D activity, which contributes to the sensitivity of cancer cells to chemotherapeutic agents.-
dc.format.extent6-
dc.language영어-
dc.language.isoENG-
dc.publisherSPANDIDOS PUBL LTD-
dc.titleAkt regulation of Aven contributes to the sensitivity of cancer cells to chemotherapeutic agents-
dc.typeArticle-
dc.publisher.location그리이스-
dc.identifier.doi10.3892/mmr.2015.3158-
dc.identifier.scopusid2-s2.0-84922324307-
dc.identifier.wosid000353849500095-
dc.identifier.bibliographicCitationMOLECULAR MEDICINE REPORTS, v.11, no.5, pp 3866 - 3871-
dc.citation.titleMOLECULAR MEDICINE REPORTS-
dc.citation.volume11-
dc.citation.number5-
dc.citation.startPage3866-
dc.citation.endPage3871-
dc.type.docTypeArticle-
dc.description.isOpenAccessN-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaOncology-
dc.relation.journalResearchAreaResearch & Experimental Medicine-
dc.relation.journalWebOfScienceCategoryOncology-
dc.relation.journalWebOfScienceCategoryMedicine, Research & Experimental-
dc.subject.keywordPlusDNA-DAMAGE-
dc.subject.keywordPlusMULTIDRUG-RESISTANCE-
dc.subject.keywordPlusPROTEIN AVEN-
dc.subject.keywordPlusPANCREATIC-CANCER-
dc.subject.keywordPlusSIGNALING PATHWAY-
dc.subject.keywordPlusTUMOR-CELLS-
dc.subject.keywordPlusMECHANISMS-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordPlusDEATH-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordAuthorAven-
dc.subject.keywordAuthorapoptosis-
dc.subject.keywordAuthorAkt-
dc.subject.keywordAuthorcathepsin D-
dc.identifier.urlhttps://www.spandidos-publications.com/10.3892/mmr.2015.3158-
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