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Conference Paper: Telomerase Activity in Leukemic Cells Is Not Related to Puromycin- and Actinomycin D-Induced Apoptosis

TitleTelomerase Activity in Leukemic Cells Is Not Related to Puromycin- and Actinomycin D-Induced Apoptosis
Authors
Issue Date1999
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSG
Citation
The 1999 Annual Physiology Symposium, Hong Kong, China, 21-22 May 1999. In Biological Signals and Receptors, 1999, v. 8 n. 3, p. 218 How to Cite?
AbstractApoptosis and cellular senescence are two forms of irreversible growth arrest which control the excessive cell growth. Deregulation of apoptosis or an escape from cellular senescence (which is an activation of telomerase) will be the crucial event driving the cells to neoplasia. It remains unclear whether there is a direct linkage between apoptosis and telomerase activity particularly in cancer cells. In the present study, we investigated telomerase activities in three leukemic cell lines (HL60, U937 and K562) after treating the cells with various doses of antitumor drugs, puromycin and actinomycin D. Our results show that the cells underwent apoptosis rapidly when treated with 20 Ìg/ml of puromycin and 5 Ìg/ml of actinomycin D, that is, about 60% of HL60 cells became apoptotic at 6 h and almost all the cells at 12 h. But telomerase activities detected by TRAP assay in these apoptotic cells remained elevated as those found in the untreated cells. However, if these cells were treated with lower dose of the drugs, i.e. 0.5–1.5 Ìg/ml of puromycin and 0.01–0.5 Ìg/ml of actinomycin D, a decrease in telomerase activity was observed at 24–48 h after addition of the drugs, and this activity could hardly be detected after 72 h. This decrease in telomerase activity was in a dose-dependent manner. Analysis of the cell cycle of these drugtreated cells by flow cytometry shows that the drugs were unselectively induced apoptosis in all phases of the cell cycle and that changes of the telomerase activity were not related to the cell cycle. Similar results were also observed in U937 and K562 cells except that K562 cells underwent apoptosis more slower than the former two cell lines. Our results suggest that apoptosis induced by puromycin and actinomycin in these three leukemic cell lines was not related to telomerase activity. The suppression of telomerase activity by low doses of the drugs is probably due to the inhibitory effect of the drugs to protein translation and RNA transcription rather than to the direct inhibition of the telomerase synthesis.
Persistent Identifierhttp://hdl.handle.net/10722/105039
ISSN
2003 Impact Factor: 3.5

 

DC FieldValueLanguage
dc.contributor.authorZhang, JXen_HK
dc.contributor.authorZhang, Zen_HK
dc.contributor.authorTsao, GSWen_HK
dc.contributor.authorLoh, TTen_HK
dc.date.accessioned2010-09-25T22:17:44Z-
dc.date.available2010-09-25T22:17:44Z-
dc.date.issued1999en_HK
dc.identifier.citationThe 1999 Annual Physiology Symposium, Hong Kong, China, 21-22 May 1999. In Biological Signals and Receptors, 1999, v. 8 n. 3, p. 218en_HK
dc.identifier.issn1422-4933en_HK
dc.identifier.urihttp://hdl.handle.net/10722/105039-
dc.description.abstractApoptosis and cellular senescence are two forms of irreversible growth arrest which control the excessive cell growth. Deregulation of apoptosis or an escape from cellular senescence (which is an activation of telomerase) will be the crucial event driving the cells to neoplasia. It remains unclear whether there is a direct linkage between apoptosis and telomerase activity particularly in cancer cells. In the present study, we investigated telomerase activities in three leukemic cell lines (HL60, U937 and K562) after treating the cells with various doses of antitumor drugs, puromycin and actinomycin D. Our results show that the cells underwent apoptosis rapidly when treated with 20 Ìg/ml of puromycin and 5 Ìg/ml of actinomycin D, that is, about 60% of HL60 cells became apoptotic at 6 h and almost all the cells at 12 h. But telomerase activities detected by TRAP assay in these apoptotic cells remained elevated as those found in the untreated cells. However, if these cells were treated with lower dose of the drugs, i.e. 0.5–1.5 Ìg/ml of puromycin and 0.01–0.5 Ìg/ml of actinomycin D, a decrease in telomerase activity was observed at 24–48 h after addition of the drugs, and this activity could hardly be detected after 72 h. This decrease in telomerase activity was in a dose-dependent manner. Analysis of the cell cycle of these drugtreated cells by flow cytometry shows that the drugs were unselectively induced apoptosis in all phases of the cell cycle and that changes of the telomerase activity were not related to the cell cycle. Similar results were also observed in U937 and K562 cells except that K562 cells underwent apoptosis more slower than the former two cell lines. Our results suggest that apoptosis induced by puromycin and actinomycin in these three leukemic cell lines was not related to telomerase activity. The suppression of telomerase activity by low doses of the drugs is probably due to the inhibitory effect of the drugs to protein translation and RNA transcription rather than to the direct inhibition of the telomerase synthesis.-
dc.languageengen_HK
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/NSGen_HK
dc.relation.ispartofBiological Signals and Receptorsen_HK
dc.rightsBiological Signals and Receptors. Copyright © S Karger AG.en_HK
dc.titleTelomerase Activity in Leukemic Cells Is Not Related to Puromycin- and Actinomycin D-Induced Apoptosisen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1422-4933&volume=8&spage=218&epage=&date=1999&atitle=Telomerase+Activity+in+Leukemic+Cells+Is+Not+Related+to+Puromycin-+and+Actinomycin+D-Induced+Apoptosisen_HK
dc.identifier.emailZhang, JX: zhangajx@hotmail.comen_HK
dc.identifier.emailLoh, TT: ttloh@hkucc.hku.hken_HK
dc.identifier.authorityZhang, JX=rp00413en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1159/000014590-
dc.identifier.hkuros44276en_HK
dc.identifier.volume8en_HK
dc.identifier.issue3-
dc.identifier.spage218en_HK
dc.identifier.epage218-

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