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dc.contributor.authorConstantinou, Andreas I.en
dc.contributor.authorKiguchi, K.en
dc.contributor.authorHuberman, E.en
dc.creatorConstantinou, Andreas I.en
dc.creatorKiguchi, K.en
dc.creatorHuberman, E.en
dc.date.accessioned2019-11-04T12:50:22Z
dc.date.available2019-11-04T12:50:22Z
dc.date.issued1990
dc.identifier.urihttp://gnosis.library.ucy.ac.cy/handle/7/52994
dc.description.abstractGenistein, an in vitro inhibitor of topoisomerase II and tyrosine kinases, suppressed growth and induced differentiation in HL-205 cells, a clonal population of the human promyelocytic HL-60 leukemia cells, and in K-562-J cells, a clonal population of the human erythroid K-562 leukemia cells. Maturing HL-205 cells acquired either granulocytic or monocytic markers, namely, reactivity with the murine OKM1 monoclonal antibody, expression of nitroblue tetrazolium dye reduction, and staining for nonspecific esterase. The maturing K-562-J cells stained with benzidine, which indicates the presence of hemoglobin, an erythroid maturation marker. Although the acquisition of the maturation markers in both HL-205 and K-562-J cells was time dependent up to 6 days, the kinetics of this induction differed between the two cell types. Despite the in vitro inhibitory effect of genistein, treatment of either HL-205 or K-562-J cells with 150 μg/ml genistein for up to 16 h did not alter topoisomerase II activity (as determined by the unknotting assay) in their nuclear extracts. Analysis with the anti-phosphotyrosine PY-20 murine monoclonal antibody indicated that treatment of K-562-J cells with genistein decreased the reactivity of the antibody with two of the cellular proteins. However, no reactivity with the PY-20 antibody was detected in untreated or genistein-treated HL-205 cells. An early event in the HL-205 and K-562-J cells, occurring after only 1 h of treatment with 30-200 μg/ml genistein, was the induction of DNA damage as measured by an alkaline elution assay. This damage may be a contributing factor in the genistein-induced cell differentiation in the HL-205 and K-562-J cells. © 1990, American Association for Cancer Research. All rights reserved.en
dc.sourceCancer researchen
dc.source.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-0025363503&partnerID=40&md5=70cf3b214bb7300d8096d9121d592354
dc.subjectarticleen
dc.subjecthumanen
dc.subjectpriority journalen
dc.subjecthuman cellen
dc.subjectDNAen
dc.subjectLeukemiaen
dc.subjectcell differentiationen
dc.subjectMolecular Weighten
dc.subjectcell strain hl 60en
dc.subjectDNA Topoisomerases, Type IIen
dc.subjectPhosphorylationen
dc.subjectleukemia cellen
dc.subjectgenisteinen
dc.subjectTumor Cells, Cultureden
dc.subjectIsoflavonesen
dc.subjectdna topoisomerase (atp hydrolysing)en
dc.subjectSupport, U.S. Gov't, Non-P.H.S.en
dc.subjectdna strand breakageen
dc.subjectDNA Damageen
dc.subjectcell strain k 562en
dc.subjectFlavonesen
dc.subjectTyrosineen
dc.titleInduction of Differentiation and DNA Strand Breakage in Human HL-60 and K-562 Leukemia Cells by Genisteinen
dc.typeinfo:eu-repo/semantics/article
dc.description.volume50
dc.description.startingpage2618
dc.description.endingpage2624
dc.author.facultyΣχολή Θετικών και Εφαρμοσμένων Επιστημών / Faculty of Pure and Applied Sciences
dc.author.departmentΤμήμα Βιολογικών Επιστημών / Department of Biological Sciences
dc.type.uhtypeArticleen
dc.description.notes<p>Manufacturers: icnen
dc.description.notesCited By :229</p>en
dc.source.abbreviationCancer Res.en
dc.contributor.orcidConstantinou, Andreas I. [0000-0003-0365-1821]
dc.gnosis.orcid0000-0003-0365-1821


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