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Article: Regulation of telomerase activity by γ-radiation in nasopharyngeal carcinoma cells

TitleRegulation of telomerase activity by γ-radiation in nasopharyngeal carcinoma cells
Authors
KeywordsNasopharyngeal carcinoma
Radiation
Telomerase
Issue Date2000
Citation
Anticancer Research, 2000, v. 20 n. 1 A, p. 433-437 How to Cite?
AbstractSince telomerase has been suggested to play a role in radiation response, the effect of radiation on the regulation of telomerase activity was studied on two NPC cell lines, CNE1 and 915. In order to investigate the correlation between cell survival and telomerase activity, three low doses (0.25, 0.5 and 1Gy) and three high doses (2, 4 and 8Gy) of γ-radiation were used. We found that low doses of radiation induced telomerase activity (up to 250% of untreated controls) followed by a cell cycle G1 arrest suggesting that the up-regulation of telomerase may play a role in initiating radiation induced cell cycle arrest. High doses of radiation resulted in decreased telomerase activity (down to 30% of untreated controls) and this was followed by an increased cell death. Our results indicate that the up-regulation of telomerase activity is an important response to radiation induced sub-lethal DNA damage. Our results also suggest that inhibition of telomerase activity by high doses of radiation may play a role radiation-induced cell death.
Persistent Identifierhttp://hdl.handle.net/10722/148201
ISSN
2023 Impact Factor: 1.6
2023 SCImago Journal Rankings: 0.562
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Xen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorChow, LSNen_HK
dc.contributor.authorWong, SCHen_HK
dc.contributor.authorTsao, GSWen_HK
dc.contributor.authorKwong, DLWen_HK
dc.contributor.authorSham, JSTen_HK
dc.contributor.authorNicholls, JMen_HK
dc.date.accessioned2012-05-29T06:11:27Z-
dc.date.available2012-05-29T06:11:27Z-
dc.date.issued2000en_HK
dc.identifier.citationAnticancer Research, 2000, v. 20 n. 1 A, p. 433-437en_HK
dc.identifier.issn0250-7005en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148201-
dc.description.abstractSince telomerase has been suggested to play a role in radiation response, the effect of radiation on the regulation of telomerase activity was studied on two NPC cell lines, CNE1 and 915. In order to investigate the correlation between cell survival and telomerase activity, three low doses (0.25, 0.5 and 1Gy) and three high doses (2, 4 and 8Gy) of γ-radiation were used. We found that low doses of radiation induced telomerase activity (up to 250% of untreated controls) followed by a cell cycle G1 arrest suggesting that the up-regulation of telomerase may play a role in initiating radiation induced cell cycle arrest. High doses of radiation resulted in decreased telomerase activity (down to 30% of untreated controls) and this was followed by an increased cell death. Our results indicate that the up-regulation of telomerase activity is an important response to radiation induced sub-lethal DNA damage. Our results also suggest that inhibition of telomerase activity by high doses of radiation may play a role radiation-induced cell death.en_HK
dc.languageengen_US
dc.relation.ispartofAnticancer Researchen_HK
dc.subjectNasopharyngeal carcinomaen_HK
dc.subjectRadiationen_HK
dc.subjectTelomeraseen_HK
dc.subject.meshCarcinoma - Enzymology - Pathologyen_US
dc.subject.meshCell Cycle - Radiation Effectsen_US
dc.subject.meshDna Damageen_US
dc.subject.meshDose-Response Relationship, Radiationen_US
dc.subject.meshEnzyme Induction - Radiation Effectsen_US
dc.subject.meshG1 Phase - Radiation Effectsen_US
dc.subject.meshGamma Raysen_US
dc.subject.meshHumansen_US
dc.subject.meshNasopharyngeal Neoplasms - Enzymology - Pathologyen_US
dc.subject.meshNeoplasm Proteins - Metabolismen_US
dc.subject.meshTelomerase - Metabolismen_US
dc.subject.meshTumor Cells, Cultured - Enzymology - Radiation Effectsen_US
dc.subject.meshTumor Stem Cell Assayen_US
dc.titleRegulation of telomerase activity by γ-radiation in nasopharyngeal carcinoma cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailTsao, GSW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailKwong, DLW:dlwkwong@hku.hken_HK
dc.identifier.emailNicholls, JM:nicholls@pathology.hku.hken_HK
dc.identifier.authorityTsao, GSW=rp00399en_HK
dc.identifier.authorityKwong, DLW=rp00414en_HK
dc.identifier.authorityNicholls, JM=rp00364en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.pmid10769692-
dc.identifier.scopuseid_2-s2.0-0034073152en_HK
dc.identifier.hkuros52814-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0034073152&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume20en_HK
dc.identifier.issue1 Aen_HK
dc.identifier.spage433en_HK
dc.identifier.epage437en_HK
dc.identifier.isiWOS:000086326500066-
dc.publisher.placeGreeceen_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridLiu, Y=26643293600en_HK
dc.identifier.scopusauthoridChow, LSN=7202533094en_HK
dc.identifier.scopusauthoridWong, SCH=7404590793en_HK
dc.identifier.scopusauthoridTsao, GSW=7102813116en_HK
dc.identifier.scopusauthoridKwong, DLW=15744231600en_HK
dc.identifier.scopusauthoridSham, JST=24472255400en_HK
dc.identifier.scopusauthoridNicholls, JM=7201463077en_HK
dc.identifier.issnl0250-7005-

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