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Novel anticancer agent, benzyldihydroxyoctenone, isolated from Streptomyces sp. causes G1 cell cycle arrest and induces apoptosis of HeLa cells

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dc.contributor.authorLee, Chul-Hoon-
dc.contributor.authorLim, Haeyoung-
dc.contributor.authorMoon, Sangik-
dc.contributor.authorShin, Choonshik-
dc.contributor.authorKim, Seunghyun-
dc.contributor.authorKim, Bum-Joon-
dc.contributor.authorLim, Yoongho-
dc.date.accessioned2010-01-11-
dc.date.available2010-01-11-
dc.date.issued2007-04-17-
dc.identifier.citationCancer Sci. 2007 Jun;98(6):795-802. Epub 2007 Apr 13.en
dc.identifier.issn1347-9032 (Print)-
dc.identifier.urihttp://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17433036-
dc.identifier.urihttps://hdl.handle.net/10371/29255-
dc.description.abstractIn the course of screening for anticancer agents, a novel active compound, F3-2-5, was isolated from culture broth of Streptomyces sp., KACC91015. Its structure was identified using nuclear magnetic resonance, mass spectrometry, and molecular modeling experiments, and confirmed by total synthesis. The growth of various human cancer cell lines was inhibited in a dose-dependent manner by 0.06-0.48 mM F3-2-5 over 24 h. Its IC(50) values were estimated at 37 microM on HeLa, 72 microM on A549, and 190 microM on HT-29 cells. However, F3-2-5 had no antiproliferative effect on normal lymphocytes and normal fibroblasts used as controls. Moreover, it affected cell cycle regulation and caused apoptosis of the HeLa cells; chromatin condensation and DNA fragmentation were observed in cells exposed to 80 microM F3-2-5. Western blot analysis revealed that F3-2-5 inhibited phosphorylation of retinoblastoma protein (pRb) and reduced expression of cyclin-dependent kinase-4 and -6, and cyclin D1 and E, while levels of p53 and p21(WAF1/CIP1) increased. Taken together, these findings show that F3-2-5 inhibits proliferation of HeLa cells by inducing G(1) phase arrest as a consequence of inhibition of pRb phosphorylation following up-regulation of p21(WAF1/CIP1) and p53. Furthermore, apoptosis in HeLa cells treated with F3-2-5 was associated with an increase in Bax and p53, leading to release of cytochrome c, activation of caspase-3, and -8, and cleavage of poly (ADP-ribose) polymerase.en
dc.language.isoen-
dc.publisherWiley-Blackwellen
dc.subjectAntineoplastic Agents/pharmacology/*therapeutic useen
dc.subjectCell Proliferation/drug effectsen
dc.subjectG1 Phase/*drug effectsen
dc.subjectHela Cellsen
dc.subjectApoptosis/*drug effectsen
dc.subjectHumansen
dc.subjectOctanols/isolation & purification/*therapeutic useen
dc.subjectPhosphorylationen
dc.subjectRetinoblastoma Protein/metabolismen
dc.subjectStreptomyces/*chemistryen
dc.subjectTumor Suppressor Protein p53/metabolismen
dc.titleNovel anticancer agent, benzyldihydroxyoctenone, isolated from Streptomyces sp. causes G1 cell cycle arrest and induces apoptosis of HeLa cellsen
dc.typeArticleen
dc.contributor.AlternativeAuthor이철훈-
dc.contributor.AlternativeAuthor임해영-
dc.contributor.AlternativeAuthor문상익-
dc.contributor.AlternativeAuthor신춘식-
dc.contributor.AlternativeAuthor김승현-
dc.contributor.AlternativeAuthor김범준-
dc.contributor.AlternativeAuthor임융호-
dc.identifier.doi10.1111/j.1349-7006.2007.00473.x-
Appears in Collections:
College of Medicine/School of Medicine (의과대학/대학원)Program in Cancer Biology (협동과정-종양생물학전공)Journal Papers (저널논문_협동과정-종양생물학전공)
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