File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Induction of stanniocalcin-1 expression in apoptotic human nasopharyngeal cancer cells by p53

TitleInduction of stanniocalcin-1 expression in apoptotic human nasopharyngeal cancer cells by p53
Authors
Issue Date2007
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/description
Citation
Biochemical And Biophysical Research Communications, 2007, v. 356 n. 4, p. 968-975 How to Cite?
AbstractThere is growing evidence to suggest that altered patterns of STC1 gene expression relate to the process of human cancer development. Our previous study has demonstrated the involvement of HIF-1 in the regulation of STC1 expression in human cancer cells. Recently, STC1 has been implicated as a putative pro-apoptotic factor in regulating the cell-death mechanism. Thus it would be of interest to know if STC1 is regulated by a tumor suppressor protein, p53. In this study, we provide evidence to demonstrate that the induction of STC1 expression in apoptotic human nasopharyngeal cancer cells (CNE2) is mediated by the activation of p53. Our study indicated that the activation of STC1 and heat-shock protein (hsp70) accompanied iodoacetamide (IDAM)-induced apoptosis in CNE-2. In addition, cellular events such as GSH depletion, mitochondrial membrane depolarization, reduction of pAkt and procaspase-3, and the induction of total p53 protein, acetylated p53, and annexin V positive cells were observed. The activation of STC1 was found to be at the transcriptional level and was independent of prior protein synthesis. Co-treatment of IDAM exposed cells with N-acetyl cysteine (NAC) prevented cell death by restoring mitochondrial membrane potential and cellular levels of GSH. NAC co-treatment also suppressed STC1 expression but had no effect on IDAM-induced hsp70 expression. RNA interference studies demonstrated that endogenous p53 was involved in activating STC1 gene expression. Collectively, the present findings provide the first evidence of p53 regulation of STC1 expression in human cancer cells. © 2007 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/183396
ISSN
2015 Impact Factor: 2.371
2015 SCImago Journal Rankings: 1.152
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLai, KPen_US
dc.contributor.authorLaw, AYSen_US
dc.contributor.authorYeung, HYen_US
dc.contributor.authorLee, LSen_US
dc.contributor.authorWagner, GFen_US
dc.contributor.authorWong, CKCen_US
dc.date.accessioned2013-05-27T07:12:33Z-
dc.date.available2013-05-27T07:12:33Z-
dc.date.issued2007en_US
dc.identifier.citationBiochemical And Biophysical Research Communications, 2007, v. 356 n. 4, p. 968-975en_US
dc.identifier.issn0006-291Xen_US
dc.identifier.urihttp://hdl.handle.net/10722/183396-
dc.description.abstractThere is growing evidence to suggest that altered patterns of STC1 gene expression relate to the process of human cancer development. Our previous study has demonstrated the involvement of HIF-1 in the regulation of STC1 expression in human cancer cells. Recently, STC1 has been implicated as a putative pro-apoptotic factor in regulating the cell-death mechanism. Thus it would be of interest to know if STC1 is regulated by a tumor suppressor protein, p53. In this study, we provide evidence to demonstrate that the induction of STC1 expression in apoptotic human nasopharyngeal cancer cells (CNE2) is mediated by the activation of p53. Our study indicated that the activation of STC1 and heat-shock protein (hsp70) accompanied iodoacetamide (IDAM)-induced apoptosis in CNE-2. In addition, cellular events such as GSH depletion, mitochondrial membrane depolarization, reduction of pAkt and procaspase-3, and the induction of total p53 protein, acetylated p53, and annexin V positive cells were observed. The activation of STC1 was found to be at the transcriptional level and was independent of prior protein synthesis. Co-treatment of IDAM exposed cells with N-acetyl cysteine (NAC) prevented cell death by restoring mitochondrial membrane potential and cellular levels of GSH. NAC co-treatment also suppressed STC1 expression but had no effect on IDAM-induced hsp70 expression. RNA interference studies demonstrated that endogenous p53 was involved in activating STC1 gene expression. Collectively, the present findings provide the first evidence of p53 regulation of STC1 expression in human cancer cells. © 2007 Elsevier Inc. All rights reserved.en_US
dc.languageengen_US
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/wps/find/journaldescription.cws_home/622790/descriptionen_US
dc.relation.ispartofBiochemical and Biophysical Research Communicationsen_US
dc.subject.meshApoptosisen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshGene Expression Regulation, Neoplasticen_US
dc.subject.meshGlycoproteins - Metabolismen_US
dc.subject.meshHumansen_US
dc.subject.meshNasopharyngeal Neoplasms - Metabolism - Pathologyen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshTumor Suppressor Protein P53 - Metabolismen_US
dc.titleInduction of stanniocalcin-1 expression in apoptotic human nasopharyngeal cancer cells by p53en_US
dc.typeArticleen_US
dc.identifier.emailLai, KP: ballllai@hotmail.comen_US
dc.identifier.authorityLai, KP=rp01753en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.bbrc.2007.03.074en_US
dc.identifier.pmid17395153-
dc.identifier.scopuseid_2-s2.0-34047114432en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34047114432&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume356en_US
dc.identifier.issue4en_US
dc.identifier.spage968en_US
dc.identifier.epage975en_US
dc.identifier.isiWOS:000245833500023-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridLai, KP=7402135707en_US
dc.identifier.scopusauthoridLaw, AYS=16175363700en_US
dc.identifier.scopusauthoridYeung, HY=7102212132en_US
dc.identifier.scopusauthoridLee, LS=35074349600en_US
dc.identifier.scopusauthoridWagner, GF=7404372679en_US
dc.identifier.scopusauthoridWong, CKC=35276549400en_US

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats