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Article: Telomerase activity is not related to apoptosis in leukemic cell lines

TitleTelomerase activity is not related to apoptosis in leukemic cell lines
Authors
KeywordsActinomycin D
Apoptosis
Flow cytometry
HL-60 cells
K562 cells
Puromycin
Telomerase
U937 cells
Issue Date2000
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescie
Citation
Life Sciences, 2000, v. 66 n. 18, p. 1713-1723 How to Cite?
AbstractAny deregulation of apoptosis or an escape from cellular senescence will drive the cells to neoplasia. It remains unclear whether there is a direct linkage between apoptosis and telomerase activity particularly in transformed cell lines. In the present study, we investigated the telomerase activities in three leukemic cell lines (HL-60, U937 and K562) after treating these cells with various doses of antitumor drugs, puromycin or actinomycin D (Act D). Our results showed that HL-60 cells underwent apoptosis rapidly when treated with either 20 μg/ml of puromycin or 5 μg/ml of Act D with more than 60% of the cells becoming apoptotic at 6 hrs and almost 100% at 12 hrs. But telomerase activity analyzed by TRAP assay in these apoptotic cells remained unchanged as compared with the untreated control cells suggesting that whether the cells were apoptotic or not, it had no effect on telomerase activity. However, if lower dosages of the drugs were used, that is, 0.5-1.5 μg/ml of puromycin or 0.01-0.5 μg/ml of Act D, a decrease in telomerase activity was observed at 24-48 hrs, and was completely undetectable at 72 hrs. This decrease in telomerase activity was dose- and time-dependent. The suppression of telomerase activity by low doses of these two drugs is probably due to the inhibitory effect of the drugs on protein translation or RNA transcription rather than direct inhibition of the telomerase activity. Flow cytometry analysis of the cell cycle of the drug-treated cells showed that these drugs unselectively induced apoptosis at all phases of the cell cycle and was unrelated to the changes in telomerase activity. Similar results were observed in U937 and K562 cells except that K562 cells underwent apoptosis more slowly than the former two cell lines.
Persistent Identifierhttp://hdl.handle.net/10722/67508
ISSN
2015 Impact Factor: 2.685
2015 SCImago Journal Rankings: 1.056
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhang, JXen_HK
dc.contributor.authorZhang, ZKen_HK
dc.contributor.authorSheng, HPen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorLoh, TTen_HK
dc.date.accessioned2010-09-06T05:55:45Z-
dc.date.available2010-09-06T05:55:45Z-
dc.date.issued2000en_HK
dc.identifier.citationLife Sciences, 2000, v. 66 n. 18, p. 1713-1723en_HK
dc.identifier.issn0024-3205en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67508-
dc.description.abstractAny deregulation of apoptosis or an escape from cellular senescence will drive the cells to neoplasia. It remains unclear whether there is a direct linkage between apoptosis and telomerase activity particularly in transformed cell lines. In the present study, we investigated the telomerase activities in three leukemic cell lines (HL-60, U937 and K562) after treating these cells with various doses of antitumor drugs, puromycin or actinomycin D (Act D). Our results showed that HL-60 cells underwent apoptosis rapidly when treated with either 20 μg/ml of puromycin or 5 μg/ml of Act D with more than 60% of the cells becoming apoptotic at 6 hrs and almost 100% at 12 hrs. But telomerase activity analyzed by TRAP assay in these apoptotic cells remained unchanged as compared with the untreated control cells suggesting that whether the cells were apoptotic or not, it had no effect on telomerase activity. However, if lower dosages of the drugs were used, that is, 0.5-1.5 μg/ml of puromycin or 0.01-0.5 μg/ml of Act D, a decrease in telomerase activity was observed at 24-48 hrs, and was completely undetectable at 72 hrs. This decrease in telomerase activity was dose- and time-dependent. The suppression of telomerase activity by low doses of these two drugs is probably due to the inhibitory effect of the drugs on protein translation or RNA transcription rather than direct inhibition of the telomerase activity. Flow cytometry analysis of the cell cycle of the drug-treated cells showed that these drugs unselectively induced apoptosis at all phases of the cell cycle and was unrelated to the changes in telomerase activity. Similar results were observed in U937 and K562 cells except that K562 cells underwent apoptosis more slowly than the former two cell lines.en_HK
dc.languageengen_HK
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/lifescieen_HK
dc.relation.ispartofLife Sciencesen_HK
dc.rightsLife Sciences. Copyright © Elsevier Inc.en_HK
dc.subjectActinomycin Den_HK
dc.subjectApoptosisen_HK
dc.subjectFlow cytometryen_HK
dc.subjectHL-60 cellsen_HK
dc.subjectK562 cellsen_HK
dc.subjectPuromycinen_HK
dc.subjectTelomeraseen_HK
dc.subjectU937 cellsen_HK
dc.subject.meshAntimetabolites, Antineoplastic - pharmacologyen_HK
dc.subject.meshApoptosis - drug effects - physiologyen_HK
dc.subject.meshDNA Fragmentation - drug effectsen_HK
dc.subject.meshDactinomycin - pharmacologyen_HK
dc.subject.meshDown-Regulation - drug effectsen_HK
dc.subject.meshFlow Cytometryen_HK
dc.subject.meshHL-60 Cellsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshK562 Cellsen_HK
dc.subject.meshLeukemia - enzymology - pathologyen_HK
dc.subject.meshPuromycin - pharmacologyen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.subject.meshTelomerase - metabolismen_HK
dc.subject.meshU937 Cellsen_HK
dc.titleTelomerase activity is not related to apoptosis in leukemic cell linesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0024-3205&volume=66&issue=18&spage=1713&epage=1723&date=2000&atitle=Telomerase+activity+is+not+related+to+apoptosis+in+leukemic+cell+linesen_HK
dc.identifier.emailZhang, JX:zhangajx@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.authorityZhang, JX=rp00413en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/S0024-3205(00)00494-Xen_HK
dc.identifier.pmid10809168-
dc.identifier.scopuseid_2-s2.0-0034708462en_HK
dc.identifier.hkuros53619en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034708462&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume66en_HK
dc.identifier.issue18en_HK
dc.identifier.spage1713en_HK
dc.identifier.epage1723en_HK
dc.identifier.isiWOS:000086161000006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridZhang, JX=12752135600en_HK
dc.identifier.scopusauthoridZhang, ZK=8560559600en_HK
dc.identifier.scopusauthoridSheng, HP=7201933542en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridLoh, TT=7102125300en_HK

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