Lovastatin-induced inhibition of HL-60 cell proliferation via cell cycle arrest and apoptosis
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Park, WH | - |
dc.contributor.author | Lee, YY | - |
dc.contributor.author | Kim, ES | - |
dc.contributor.author | Seol, JG | - |
dc.contributor.author | Jung, CW | - |
dc.contributor.author | Lee, CC | - |
dc.contributor.author | Kim, BK | - |
dc.date.accessioned | 2021-06-18T14:44:47Z | - |
dc.date.available | 2021-06-18T14:44:47Z | - |
dc.date.issued | 1999-07 | - |
dc.identifier.issn | 0250-7005 | - |
dc.identifier.issn | 1791-7530 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/cau/handle/2019.sw.cau/47438 | - |
dc.description.abstract | An inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, lovastatin, induces growth arrest and cell death in a wide variety of malignant cells in vitro. We analyzed the effect of lovastatin on. myeloid leukemic cell lines. Lovastatin significantly inhibited the proliferation of 7 cell lines among II myeloid leukemic cell lines in a dose-dependent manner: In order to address the mechanism of antileukemic effect of lovastatin, cell cycle analysis was attempted in HL-60 cells, showing that lovastatin induced GI nn est in HL-60 cells following 72 h of drug exposure (1.5 mu M, 5 mu M and 10 mu M) in a dose-dependent manna: Analysis of GI regulatory proteins demonstrated that the protein levels of cyclin-dependent kinase (CDK) 5 CDK4, CDK6 and cyclin E were decreased after treatment with lovastatin (10 mu M) in a time-dependent manner, but not cyclin DI. In addition lovastatin increased the protein level of the cyclin-dependent kinase inhibitor (CDKI), p27, and markedly enhanced the binding of p27 with CDK2 and CDK4 more than CDK6 after 24 h exposure. At higher doses of lovastatin (50 mM 100 mM, 200 mM), a significant apoptosis was observed as evidenced by FAGS analysis with annexin V staining, which was associated with downregulation of Bcl-2 protein. These results suggest that lovastatin inhibits the proliferation of myeloid leukemic cells via GI arrest in association with p27 induction and is an effective inducer of apoptosis in HL-60 cells. | - |
dc.format.extent | 8 | - |
dc.language | 영어 | - |
dc.language.iso | ENG | - |
dc.publisher | INT INST ANTICANCER RESEARCH | - |
dc.title | Lovastatin-induced inhibition of HL-60 cell proliferation via cell cycle arrest and apoptosis | - |
dc.type | Article | - |
dc.identifier.bibliographicCitation | ANTICANCER RESEARCH, v.19, no.4B, pp 3133 - 3140 | - |
dc.description.isOpenAccess | N | - |
dc.identifier.wosid | 000084768100043 | - |
dc.identifier.scopusid | 2-s2.0-0033451446 | - |
dc.citation.endPage | 3140 | - |
dc.citation.number | 4B | - |
dc.citation.startPage | 3133 | - |
dc.citation.title | ANTICANCER RESEARCH | - |
dc.citation.volume | 19 | - |
dc.type.docType | Article | - |
dc.publisher.location | 그리이스 | - |
dc.subject.keywordAuthor | lovastatin | - |
dc.subject.keywordAuthor | cell cycle | - |
dc.subject.keywordAuthor | cyclin-dependent kinase inhibitor | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | HL-60 | - |
dc.subject.keywordPlus | MEVALONATE PATHWAY | - |
dc.subject.keywordPlus | DEPENDENT KINASES | - |
dc.subject.keywordPlus | LEUKEMIA-CELLS | - |
dc.subject.keywordPlus | CULTURED-CELLS | - |
dc.subject.keywordPlus | RAS FUNCTION | - |
dc.subject.keywordPlus | GROWTH | - |
dc.subject.keywordPlus | CHOLESTEROL | - |
dc.subject.keywordPlus | PROTEINS | - |
dc.subject.keywordPlus | PHOSPHATIDYLSERINE | - |
dc.subject.keywordPlus | IDENTIFICATION | - |
dc.relation.journalResearchArea | Oncology | - |
dc.relation.journalWebOfScienceCategory | Oncology | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
Items in ScholarWorks are protected by copyright, with all rights reserved, unless otherwise indicated.
84, Heukseok-ro, Dongjak-gu, Seoul, Republic of Korea (06974)02-820-6194
COPYRIGHT 2019 Chung-Ang University All Rights Reserved.
Certain data included herein are derived from the © Web of Science of Clarivate Analytics. All rights reserved.
You may not copy or re-distribute this material in whole or in part without the prior written consent of Clarivate Analytics.