Cell cycle arrest and apoptotic induction in LNCaP cells by MCS-C2, novel cyclin-dependent kinase inhibitor, through p53/p21(WAF1/CIP1) pathway
DC Field | Value | Language |
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dc.contributor.author | Park, Hae Young | - |
dc.contributor.author | Kim, Min Kyoung | - |
dc.contributor.author | Moon, Sang-Ik | - |
dc.contributor.author | Cho, Youl-Hee | - |
dc.contributor.author | Lee, Chul-Hoon | - |
dc.date.accessioned | 2021-06-23T21:41:03Z | - |
dc.date.available | 2021-06-23T21:41:03Z | - |
dc.date.issued | 2006-05 | - |
dc.identifier.issn | 1347-9032 | - |
dc.identifier.issn | 1349-7006 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/erica/handle/2021.sw.erica/44941 | - |
dc.description.abstract | The 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. | - |
dc.format.extent | 7 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | Oxford University Press | - |
dc.title | Cell cycle arrest and apoptotic induction in LNCaP cells by MCS-C2, novel cyclin-dependent kinase inhibitor, through p53/p21(WAF1/CIP1) pathway | - |
dc.type | Article | - |
dc.publisher.location | 미국 | - |
dc.identifier.doi | 10.1111/j.1349-7006.2006.00195.x | - |
dc.identifier.scopusid | 2-s2.0-33645545037 | - |
dc.identifier.wosid | 000236585400014 | - |
dc.identifier.bibliographicCitation | Cancer Science, v.97, no.5, pp 430 - 436 | - |
dc.citation.title | Cancer Science | - |
dc.citation.volume | 97 | - |
dc.citation.number | 5 | - |
dc.citation.startPage | 430 | - |
dc.citation.endPage | 436 | - |
dc.type.docType | Article | - |
dc.description.isOpenAccess | N | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.subject.keywordPlus | ANTIVIRAL ACTIVITY | - |
dc.subject.keywordPlus | LEUKEMIA-CELLS | - |
dc.subject.keywordPlus | P53 | - |
dc.subject.keywordPlus | TOYOCAMYCIN | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
dc.subject.keywordPlus | IDENTIFICATION | - |
dc.subject.keywordPlus | PROGRESSION | - |
dc.subject.keywordPlus | CLEAVAGE | - |
dc.subject.keywordPlus | PROMOTES | - |
dc.subject.keywordPlus | ANALOGS | - |
dc.identifier.url | https://onlinelibrary.wiley.com/doi/10.1111/j.1349-7006.2006.00195.x | - |
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