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Article: Inhibition of human telomerase reverse transcriptase by nonsteroidal antiinflammatory drugs in colon carcinoma

TitleInhibition of human telomerase reverse transcriptase by nonsteroidal antiinflammatory drugs in colon carcinoma
Authors
KeywordsAspirin
Cyclooxygenase
Human telomerase reverse transcriptase
Indomethacin
Nonsteroidal antiinflammatory drugs
SC-236
Telomerase
Issue Date2006
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741
Citation
Cancer, 2006, v. 106 n. 6, p. 1243-1249 How to Cite?
AbstractBACKGROUND. Telomerase activation, which is observed in most human cancers, plays an important role in carcinogenesis. Human telomerase reverse transcriptase (hTERT) is a subunit of telomerase that is essential for telomerase activity. The aim of the study was to investigate whether nonsteroidal antiinflammatory drugs (NSAIDs) inhibit telomerase activity and hTERT. METHODS. Four colon carcinoma cell lines, HT-29, COLO205, CRL-2134, and SW1116, were used in the experiments. Polymerase chain reaction-based telomeric repeat amplification (TRAP) enzyme-linked immunosorbent assay (ELISA) was used to measure telomerase activity in the cells after treatment with aspirin, indomethacin, or SC-236 (a specific cyclooxygenase-2 [COX-2] inhibitor). Expression of hTERT mRNA and protein was detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, respectively. The dual luciferase reporter assay was performed to identify the potential cis-response elements to NSAIDs in the promoter region of hTERT. RESULTS. Aspirin, indomethacin, and SC-236 inhibited telomerase activity in HT-29, COLO205, and CRL-2134 cell lines, but not in the SW1116 cell line. NSAIDs inhibited hTERT mRNA and protein expression through suppression of hTERT transcriptional activity. The hTERT promoter fragment -145 to -330 basepairs (bp) upstream of the ATG starting site was sufficient to respond to the NSAID-induced inhibitory effect and the inhibition was COX-2-independent. CONCLUSION. NSAIDs inhibit telomerase activity at hTERT transcriptional, mRNA, and protein levels in colon carcinoma cells. The hTERT promoter fragment -145 to -330 bp may be the cis-response element to NSAIDs. © 2006 American Cancer Society.
Persistent Identifierhttp://hdl.handle.net/10722/70301
ISSN
2015 Impact Factor: 5.649
2015 SCImago Journal Rankings: 3.188
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHe, Hen_HK
dc.contributor.authorXia, HHXen_HK
dc.contributor.authorDe Wang, Jen_HK
dc.contributor.authorGu, Qen_HK
dc.contributor.authorLin, MCMen_HK
dc.contributor.authorZou, Ben_HK
dc.contributor.authorLam, SKen_HK
dc.contributor.authorChan, AOOen_HK
dc.contributor.authorYuen, MFen_HK
dc.contributor.authorKung, HFen_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2010-09-06T06:21:35Z-
dc.date.available2010-09-06T06:21:35Z-
dc.date.issued2006en_HK
dc.identifier.citationCancer, 2006, v. 106 n. 6, p. 1243-1249en_HK
dc.identifier.issn0008-543Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/70301-
dc.description.abstractBACKGROUND. Telomerase activation, which is observed in most human cancers, plays an important role in carcinogenesis. Human telomerase reverse transcriptase (hTERT) is a subunit of telomerase that is essential for telomerase activity. The aim of the study was to investigate whether nonsteroidal antiinflammatory drugs (NSAIDs) inhibit telomerase activity and hTERT. METHODS. Four colon carcinoma cell lines, HT-29, COLO205, CRL-2134, and SW1116, were used in the experiments. Polymerase chain reaction-based telomeric repeat amplification (TRAP) enzyme-linked immunosorbent assay (ELISA) was used to measure telomerase activity in the cells after treatment with aspirin, indomethacin, or SC-236 (a specific cyclooxygenase-2 [COX-2] inhibitor). Expression of hTERT mRNA and protein was detected by reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting, respectively. The dual luciferase reporter assay was performed to identify the potential cis-response elements to NSAIDs in the promoter region of hTERT. RESULTS. Aspirin, indomethacin, and SC-236 inhibited telomerase activity in HT-29, COLO205, and CRL-2134 cell lines, but not in the SW1116 cell line. NSAIDs inhibited hTERT mRNA and protein expression through suppression of hTERT transcriptional activity. The hTERT promoter fragment -145 to -330 basepairs (bp) upstream of the ATG starting site was sufficient to respond to the NSAID-induced inhibitory effect and the inhibition was COX-2-independent. CONCLUSION. NSAIDs inhibit telomerase activity at hTERT transcriptional, mRNA, and protein levels in colon carcinoma cells. The hTERT promoter fragment -145 to -330 bp may be the cis-response element to NSAIDs. © 2006 American Cancer Society.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jhome/28741en_HK
dc.relation.ispartofCanceren_HK
dc.rightsCancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectAspirinen_HK
dc.subjectCyclooxygenaseen_HK
dc.subjectHuman telomerase reverse transcriptaseen_HK
dc.subjectIndomethacinen_HK
dc.subjectNonsteroidal antiinflammatory drugsen_HK
dc.subjectSC-236en_HK
dc.subjectTelomeraseen_HK
dc.subject.meshAdenocarcinoma - drug therapy - enzymology - geneticsen_HK
dc.subject.meshAnti-Inflammatory Agents, Non-Steroidal - pharmacologyen_HK
dc.subject.meshAspirin - pharmacologyen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshColonic Neoplasms - drug therapy - enzymology - geneticsen_HK
dc.subject.meshCyclooxygenase 2 - chemistry - metabolismen_HK
dc.subject.meshCyclooxygenase Inhibitors - pharmacologyen_HK
dc.subject.meshDNA-Binding Proteins - antagonists & inhibitors - genetics - metabolismen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIndomethacin - pharmacologyen_HK
dc.subject.meshLuciferases - metabolismen_HK
dc.subject.meshPromoter Regions, Genetic - geneticsen_HK
dc.subject.meshPyrazoles - pharmacologyen_HK
dc.subject.meshRNA, Messenger - genetics - metabolismen_HK
dc.subject.meshRNA, Neoplasmen_HK
dc.subject.meshResponse Elementsen_HK
dc.subject.meshSulfonamides - pharmacologyen_HK
dc.subject.meshTelomerase - antagonists & inhibitors - genetics - metabolismen_HK
dc.subject.meshTranscription, Geneticen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.titleInhibition of human telomerase reverse transcriptase by nonsteroidal antiinflammatory drugs in colon carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-543X&volume=106&issue=6&spage=1243&epage=9&date=2006&atitle=Inhibition+of+human+telomerase+reverse+transcriptase+by+nonsteroidal+antiinflammatory+drugs+in+colon+carcinomaen_HK
dc.identifier.emailDe Wang, J: jidewang@gmail.comen_HK
dc.identifier.emailLin, MCM: mcllin@hkucc.hku.hken_HK
dc.identifier.emailYuen, MF: mfyuen@hku.hken_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityDe Wang, J=rp00491en_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.identifier.authorityYuen, MF=rp00479en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/cncr.21694en_HK
dc.identifier.pmid16444744en_HK
dc.identifier.scopuseid_2-s2.0-33644833354en_HK
dc.identifier.hkuros114980en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33644833354&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume106en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1243en_HK
dc.identifier.epage1249en_HK
dc.identifier.isiWOS:000236019500006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHe, H=36185495900en_HK
dc.identifier.scopusauthoridXia, HHX=8757161400en_HK
dc.identifier.scopusauthoridDe Wang, J=35309087500en_HK
dc.identifier.scopusauthoridGu, Q=24469982400en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK
dc.identifier.scopusauthoridZou, B=35228257300en_HK
dc.identifier.scopusauthoridLam, SK=7402279800en_HK
dc.identifier.scopusauthoridChan, AOO=7403167965en_HK
dc.identifier.scopusauthoridYuen, MF=7102031955en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK

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