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dc.contributor.author이철훈-
dc.date.accessioned2019-07-31T06:21:30Z-
dc.date.available2019-07-31T06:21:30Z-
dc.date.issued2006-05-
dc.identifier.citationCANCER SCIENCE, v. 97, No. 5, Page. 430-436en_US
dc.identifier.issn1349-7006-
dc.identifier.urihttps://onlinelibrary.wiley.com/doi/full/10.1111/j.1349-7006.2006.00195.x-
dc.identifier.urihttp://repository.hanyang.ac.kr/handle/20.500.11754/108052-
dc.description.abstractThe purpose of the present study was to investigate the mechanisms involved in the antiproliferative and apoptotic effects of MCS-C2, a novel analog of the pyrrolo[2,3-d]pyrimidine nucleoside toyocamycin and sangivamycin, in human prostate cancer LNCaP cells. MCS-C2, a selective inhibitor of cyclin-dependent kinase, was found to inhibit cell growth in a time- and dose-dependent manner, and inhibit cell cycle progression by inducing the arrest of the G1 phase and apoptosis in LNCaP cells. When treated with 3 mu M MCS-C2, inhibited proliferation associated with apoptotic induction was found in the LNCaP cells in a concentration and time-dependent manner, and nuclear DAPI staining revealed the typical nuclear features of apoptosis. Furthermore, MCS-C2 induced cell cycle arrest in the G1 phase through the upregulated phosphorylation of the p53 protein at Ser-15 and activation of its downstream target gene p21(WAF1/CIP1). Accordingly, these results suggest that MCS-C2 inhibits the proliferation of LNCaP cells by way of G1-phase arrest and apoptosis in association with the regulation of multiple molecules in the cell cycle progression.en_US
dc.description.sponsorshipThis work was supported by research funding from Hanyang University (HY‐2002‐I) and by grant no. R01‐2003‐000‐10594‐0 from the Basic Research Program of the Korea Science and Engineering Foundation.en_US
dc.language.isoen_USen_US
dc.publisherBUSINESS CENTER ACADEMIC SOCIETIES JAPANen_US
dc.titleCell cycle arrest and apoptotic induction in LNCaP cells by MCS-C2, novel cyclin-dependent kinase inhibitor, through p53/p21(WAF1/CIP1) pathwayen_US
dc.typeArticleen_US
dc.identifier.doi10.1111/j.1349-7006.2006.00195.x-
dc.relation.journalCANCER SCIENCE-
dc.contributor.googleauthorPark, HY-
dc.contributor.googleauthorKim, MK-
dc.contributor.googleauthorMoon, SI-
dc.contributor.googleauthorCho, YH-
dc.contributor.googleauthorLee, CH-
dc.relation.code2009211563-
dc.sector.campusE-
dc.sector.daehakCOLLEGE OF PHARMACY[E]-
dc.sector.departmentDEPARTMENT OF PHARMACY-
dc.identifier.pidchhlee-
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COLLEGE OF PHARMACY[E](약학대학) > PHARMACY(약학과) > Articles
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