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Article: Upregulation of GADD153 expression in the apoptotic signaling of N-(4-hydroxyphenyl)retinamide (4HPR)

TitleUpregulation of GADD153 expression in the apoptotic signaling of N-(4-hydroxyphenyl)retinamide (4HPR)
Authors
Issue Date2002
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal Of Cancer, 2002, v. 102 n. 1, p. 7-14 How to Cite?
AbstractThe molecular basis for the pharmacologic effects of N-(4-hydroxyphenyl)retinamide (4HPR) was investigated by studying the gene(s) that this compound may upregulate in cultured human epithelial tumor cells. Treatment of the cultured human nasopharyngeal carcinoma-derived cells (CNE3) with 4HPR caused modest cell-cycle arrest at G1 and apoptosis. The mRNA levels of a total of 20 genes were downregulated with the majority of them involved in cell cycle-related functions. Only the mRNA level of the growth arrest and DNA-damage inducible gene (gadd153) was upregulated by approximately 7-fold, with a concomitant increase in intracellular protein level. Similar upregulation of gadd153 by 4HPR was observed in HeLa and 2 other tumor cell lines. The 4HPR-induced apoptosis was markedly enhanced in the CNE3 cells that transiently overexpressed the gadd153 protein. Unlike 4HPR, all-trans-retinoic acid (ATRA) had no effect on the mRNA or protein level of gadd153 . The ability of 4HPR and ATRA to stimulate the promoter activity ofgaddl53 was then examined. In the HeLa cells, both 4HPR and ATRA caused a 2- to 4-fold stimulation of the promoter activity of gaddl53, but similar to the CNE3 cells, ATRA was incapable of upregulating the protein level of gaddl53. This is the first demonstration that gadd153 is a 4HPR-responsive gene in tumor cells and may have a functional role to play in 4HPR-induced apoptosis. Furthermore, our data suggest that the expression of gadd153 can be regulated by 4HPR at the transcriptional level. © 2002 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/68135
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXia, Yen_HK
dc.contributor.authorWong, NSen_HK
dc.contributor.authorFong, WFen_HK
dc.contributor.authorTideman, Hen_HK
dc.date.accessioned2010-09-06T06:01:42Z-
dc.date.available2010-09-06T06:01:42Z-
dc.date.issued2002en_HK
dc.identifier.citationInternational Journal Of Cancer, 2002, v. 102 n. 1, p. 7-14en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/68135-
dc.description.abstractThe molecular basis for the pharmacologic effects of N-(4-hydroxyphenyl)retinamide (4HPR) was investigated by studying the gene(s) that this compound may upregulate in cultured human epithelial tumor cells. Treatment of the cultured human nasopharyngeal carcinoma-derived cells (CNE3) with 4HPR caused modest cell-cycle arrest at G1 and apoptosis. The mRNA levels of a total of 20 genes were downregulated with the majority of them involved in cell cycle-related functions. Only the mRNA level of the growth arrest and DNA-damage inducible gene (gadd153) was upregulated by approximately 7-fold, with a concomitant increase in intracellular protein level. Similar upregulation of gadd153 by 4HPR was observed in HeLa and 2 other tumor cell lines. The 4HPR-induced apoptosis was markedly enhanced in the CNE3 cells that transiently overexpressed the gadd153 protein. Unlike 4HPR, all-trans-retinoic acid (ATRA) had no effect on the mRNA or protein level of gadd153 . The ability of 4HPR and ATRA to stimulate the promoter activity ofgaddl53 was then examined. In the HeLa cells, both 4HPR and ATRA caused a 2- to 4-fold stimulation of the promoter activity of gaddl53, but similar to the CNE3 cells, ATRA was incapable of upregulating the protein level of gaddl53. This is the first demonstration that gadd153 is a 4HPR-responsive gene in tumor cells and may have a functional role to play in 4HPR-induced apoptosis. Furthermore, our data suggest that the expression of gadd153 can be regulated by 4HPR at the transcriptional level. © 2002 Wiley-Liss, Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_HK
dc.relation.ispartofInternational Journal of Canceren_HK
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshAntineoplastic Agents - pharmacologyen_HK
dc.subject.meshApoptosis - drug effectsen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshCCAAT-Enhancer-Binding Proteins - genetics - metabolismen_HK
dc.subject.meshCell Cycle - drug effectsen_HK
dc.subject.meshCell Division - drug effectsen_HK
dc.subject.meshDNA Primers - chemistryen_HK
dc.subject.meshFenretinide - pharmacologyen_HK
dc.subject.meshFlow Cytometryen_HK
dc.subject.meshGene Expression Profilingen_HK
dc.subject.meshGene Expression Regulationen_HK
dc.subject.meshHumansen_HK
dc.subject.meshLuciferases - metabolismen_HK
dc.subject.meshMicroscopy, Fluorescenceen_HK
dc.subject.meshNeoplasms, Glandular and Epithelial - drug therapy - metabolism - pathologyen_HK
dc.subject.meshOligonucleotide Array Sequence Analysisen_HK
dc.subject.meshPlasmidsen_HK
dc.subject.meshPolymerase Chain Reactionen_HK
dc.subject.meshRNA, Messenger - metabolismen_HK
dc.subject.meshReceptors, Retinoic Acid - metabolismen_HK
dc.subject.meshTranscription Factor CHOPen_HK
dc.subject.meshTranscription Factors - genetics - metabolismen_HK
dc.subject.meshTretinoin - pharmacologyen_HK
dc.subject.meshTumor Cells, Cultured - drug effectsen_HK
dc.subject.meshUp-Regulationen_HK
dc.titleUpregulation of GADD153 expression in the apoptotic signaling of N-(4-hydroxyphenyl)retinamide (4HPR)en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0020-7136&volume=102&issue=1&spage=7&epage=14&date=2002&atitle=Upregulation+of+GADD153+expression+in+the+apoptotic+signaling+of+N-(4-hydroxyphenyl)retinamide+(4HPR)en_HK
dc.identifier.emailWong, NS:nswong@hkucc.hku.hken_HK
dc.identifier.authorityWong, NS=rp00340en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.10664en_HK
dc.identifier.pmid12353227-
dc.identifier.scopuseid_2-s2.0-0036837429en_HK
dc.identifier.hkuros81140en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036837429&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume102en_HK
dc.identifier.issue1en_HK
dc.identifier.spage7en_HK
dc.identifier.epage14en_HK
dc.identifier.isiWOS:000178437500002-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridXia, Y=36986179900en_HK
dc.identifier.scopusauthoridWong, NS=7202836641en_HK
dc.identifier.scopusauthoridFong, WF=7102816013en_HK
dc.identifier.scopusauthoridTideman, H=7005602469en_HK

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