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Article: ROS mediates 4HPR-induced posttranscriptional expression of the Gadd153 gene

TitleROS mediates 4HPR-induced posttranscriptional expression of the Gadd153 gene
Authors
Issue Date2005
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomed
Citation
Free Radical Biology And Medicine, 2005, v. 38 n. 12, p. 1585-1593 How to Cite?
AbstractAll-trans-N-(4-hydroxyphenyl)retinamide (4HPR) is a synthetic retinoid that can induce apoptosis in many cancer cell lines. The cytotoxicity of 4HPR is dependent on the production of ROS but the underlying reasons are not entirely certain. We have investigated the role of 4HPR-induced production of ROS in mediating the expression of the recently identified 4HPR-responsive gene Gadd153. In 4HPR-treated cells, the elevation of Gadd153 protein level was prevented by vitamin C, which had no effect on the activation of the Gadd153 gene promoter. The 4HPR-induced elevation of Gadd153 mRNA level persisted even after transcription was blocked with actinomycin D, but declined rapidly upon the addition of antioxidants to the transcription-arrested cells. The mRNA expressed from the full-length Gadd153 cDNA was degraded constitutively in cells in the absence but not in the presence of 4HPR. Such an inhibitory effect of 4HPR was abolished by antioxidants and by inhibitors of 12-lipoxygenase, baicalein (specific) and esculetin (panspecific). The inhibition of 4HPR-induced expression of Gadd153 protein by vitamin C was independent of intracellular proteasome activity and vitamin C had no effect on the intracellular decay of Gadd153 protein. Our data provide the first evidence that the posttranscriptional expression of the Gadd153 gene can be regulated by ROS produced by 4HPR. © 2005 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/147514
ISSN
2015 Impact Factor: 5.784
2015 SCImago Journal Rankings: 2.468
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, WLen_US
dc.contributor.authorWong, NSen_US
dc.date.accessioned2012-05-29T06:04:16Z-
dc.date.available2012-05-29T06:04:16Z-
dc.date.issued2005en_US
dc.identifier.citationFree Radical Biology And Medicine, 2005, v. 38 n. 12, p. 1585-1593en_US
dc.identifier.issn0891-5849en_US
dc.identifier.urihttp://hdl.handle.net/10722/147514-
dc.description.abstractAll-trans-N-(4-hydroxyphenyl)retinamide (4HPR) is a synthetic retinoid that can induce apoptosis in many cancer cell lines. The cytotoxicity of 4HPR is dependent on the production of ROS but the underlying reasons are not entirely certain. We have investigated the role of 4HPR-induced production of ROS in mediating the expression of the recently identified 4HPR-responsive gene Gadd153. In 4HPR-treated cells, the elevation of Gadd153 protein level was prevented by vitamin C, which had no effect on the activation of the Gadd153 gene promoter. The 4HPR-induced elevation of Gadd153 mRNA level persisted even after transcription was blocked with actinomycin D, but declined rapidly upon the addition of antioxidants to the transcription-arrested cells. The mRNA expressed from the full-length Gadd153 cDNA was degraded constitutively in cells in the absence but not in the presence of 4HPR. Such an inhibitory effect of 4HPR was abolished by antioxidants and by inhibitors of 12-lipoxygenase, baicalein (specific) and esculetin (panspecific). The inhibition of 4HPR-induced expression of Gadd153 protein by vitamin C was independent of intracellular proteasome activity and vitamin C had no effect on the intracellular decay of Gadd153 protein. Our data provide the first evidence that the posttranscriptional expression of the Gadd153 gene can be regulated by ROS produced by 4HPR. © 2005 Elsevier Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/freeradbiomeden_US
dc.relation.ispartofFree Radical Biology and Medicineen_US
dc.subject.meshAntioxidants - Pharmacologyen_US
dc.subject.meshAscorbic Acid - Pharmacologyen_US
dc.subject.meshCcaat-Enhancer-Binding Proteins - Biosynthesisen_US
dc.subject.meshDactinomycin - Pharmacologyen_US
dc.subject.meshFenretinide - Pharmacologyen_US
dc.subject.meshFlavanones - Pharmacologyen_US
dc.subject.meshHt29 Cellsen_US
dc.subject.meshHela Cellsen_US
dc.subject.meshHumansen_US
dc.subject.meshLipoxygenase Inhibitors - Pharmacologyen_US
dc.subject.meshPromoter Regions, Genetic - Drug Effectsen_US
dc.subject.meshRna, Messenger - Drug Effectsen_US
dc.subject.meshReactive Oxygen Species - Metabolismen_US
dc.subject.meshTranscription Factor Chopen_US
dc.subject.meshTranscription Factors - Biosynthesisen_US
dc.subject.meshTranscription, Genetic - Drug Effectsen_US
dc.subject.meshUmbelliferones - Pharmacologyen_US
dc.titleROS mediates 4HPR-induced posttranscriptional expression of the Gadd153 geneen_US
dc.typeArticleen_US
dc.identifier.emailWong, NS:nswong@hkucc.hku.hken_US
dc.identifier.authorityWong, NS=rp00340en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.freeradbiomed.2005.02.024en_US
dc.identifier.pmid15917187-
dc.identifier.scopuseid_2-s2.0-19444370770en_US
dc.identifier.hkuros102123-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-19444370770&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume38en_US
dc.identifier.issue12en_US
dc.identifier.spage1585en_US
dc.identifier.epage1593en_US
dc.identifier.isiWOS:000229666100005-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLai, WL=8563343400en_US
dc.identifier.scopusauthoridWong, NS=7202836641en_US

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