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- PMID: 12353227
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Article: Upregulation of GADD153 expression in the apoptotic signaling of N-(4-hydroxyphenyl)retinamide (4HPR)
Title | Upregulation of GADD153 expression in the apoptotic signaling of N-(4-hydroxyphenyl)retinamide (4HPR) |
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Authors | |
Keywords | 4-Hydroxyphenyl)retinamide Apoptosis Cell cycle Gadd153 |
Issue Date | 2002 |
Publisher | John 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? |
Abstract | The 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 Identifier | http://hdl.handle.net/10722/68135 |
ISSN | 2023 Impact Factor: 5.7 2023 SCImago Journal Rankings: 2.131 |
ISI Accession Number ID | |
References |
DC Field | Value | Language |
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dc.contributor.author | Xia, Y | en_HK |
dc.contributor.author | Wong, NS | en_HK |
dc.contributor.author | Fong, WF | en_HK |
dc.contributor.author | Tideman, H | en_HK |
dc.date.accessioned | 2010-09-06T06:01:42Z | - |
dc.date.available | 2010-09-06T06:01:42Z | - |
dc.date.issued | 2002 | en_HK |
dc.identifier.citation | International Journal Of Cancer, 2002, v. 102 n. 1, p. 7-14 | en_HK |
dc.identifier.issn | 0020-7136 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/68135 | - |
dc.description.abstract | The 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.language | eng | en_HK |
dc.publisher | John Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home | en_HK |
dc.relation.ispartof | International Journal of Cancer | en_HK |
dc.rights | International Journal of Cancer. Copyright © John Wiley & Sons, Inc. | en_HK |
dc.subject | 4-Hydroxyphenyl)retinamide | - |
dc.subject | Apoptosis | - |
dc.subject | Cell cycle | - |
dc.subject | Gadd153 | - |
dc.subject.mesh | Antineoplastic Agents - pharmacology | en_HK |
dc.subject.mesh | Apoptosis - drug effects | en_HK |
dc.subject.mesh | Blotting, Western | en_HK |
dc.subject.mesh | CCAAT-Enhancer-Binding Proteins - genetics - metabolism | en_HK |
dc.subject.mesh | Cell Cycle - drug effects | en_HK |
dc.subject.mesh | Cell Division - drug effects | en_HK |
dc.subject.mesh | DNA Primers - chemistry | en_HK |
dc.subject.mesh | Fenretinide - pharmacology | en_HK |
dc.subject.mesh | Flow Cytometry | en_HK |
dc.subject.mesh | Gene Expression Profiling | en_HK |
dc.subject.mesh | Gene Expression Regulation | en_HK |
dc.subject.mesh | Humans | en_HK |
dc.subject.mesh | Luciferases - metabolism | en_HK |
dc.subject.mesh | Microscopy, Fluorescence | en_HK |
dc.subject.mesh | Neoplasms, Glandular and Epithelial - drug therapy - metabolism - pathology | en_HK |
dc.subject.mesh | Oligonucleotide Array Sequence Analysis | en_HK |
dc.subject.mesh | Plasmids | en_HK |
dc.subject.mesh | Polymerase Chain Reaction | en_HK |
dc.subject.mesh | RNA, Messenger - metabolism | en_HK |
dc.subject.mesh | Receptors, Retinoic Acid - metabolism | en_HK |
dc.subject.mesh | Transcription Factor CHOP | en_HK |
dc.subject.mesh | Transcription Factors - genetics - metabolism | en_HK |
dc.subject.mesh | Tretinoin - pharmacology | en_HK |
dc.subject.mesh | Tumor Cells, Cultured - drug effects | en_HK |
dc.subject.mesh | Up-Regulation | en_HK |
dc.title | Upregulation of GADD153 expression in the apoptotic signaling of N-(4-hydroxyphenyl)retinamide (4HPR) | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://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.email | Wong, NS:nswong@hkucc.hku.hk | en_HK |
dc.identifier.authority | Wong, NS=rp00340 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1002/ijc.10664 | en_HK |
dc.identifier.pmid | 12353227 | - |
dc.identifier.scopus | eid_2-s2.0-0036837429 | en_HK |
dc.identifier.hkuros | 81140 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-0036837429&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 102 | en_HK |
dc.identifier.issue | 1 | en_HK |
dc.identifier.spage | 7 | en_HK |
dc.identifier.epage | 14 | en_HK |
dc.identifier.isi | WOS:000178437500002 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Xia, Y=36986179900 | en_HK |
dc.identifier.scopusauthorid | Wong, NS=7202836641 | en_HK |
dc.identifier.scopusauthorid | Fong, WF=7102816013 | en_HK |
dc.identifier.scopusauthorid | Tideman, H=7005602469 | en_HK |
dc.identifier.issnl | 0020-7136 | - |