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Article: A possible role of cIAP2 in Helicobacter pylori-associated gastric cancer

TitleA possible role of cIAP2 in Helicobacter pylori-associated gastric cancer
Authors
Li, ZChen, JChan, KWQiao, LWong, BCY
KeywordsCarcinogenesis
CIAP2
Gastric cancer
Gene therapy
Helicobacter pylori
Issue Date2011
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2011, v. 313 n. 2, p. 192-200 How to Cite?
DOI: http://dx.doi.org/10.1016/j.canlet.2011.09.007
AbstractCellular inhibitor of apoptosis protein 2 (cIAP2) is a member of the IAP family and is over-expressed in most cancer tissues. In this study, we investigated the role cIAP2 in Helicobacter pylori (HP) related gastric carcinogenesis. We measured the expression of cIAP2 at mRNA and protein levels in a panel of gastric cancer cell lines and human gastric cancer tissues by semi-quantitative reverse transcriptase PCR (RT-PCR), quantitative real time PCR (qPCR), immunoblotting, and immunohistochemistry. The effects of cIAP2 down-regulation on gastric cell proliferation and apoptosis were detected by standard WST-1 assay and flow cytometry, respectively. Infection of gastric mucosa by HP enhances the expression of cIAP2 in mouse gastric tissues. Over 70% of human gastric cancer tissues express higher amount of cIAP2. Well-differentiated gastric cancer cells express more cIAP2 than moderately- and poorly-differentiated gastric cancer cells. Knocking down of cIAP2 in SGC-7901 cells results in a 30% decrease in cell proliferation, a 20% increase in apoptosis and delayed migration. Thus, cIAP2 may play an important role in HP-induced gastric carcinogenesis, and it may serve as a potential target for gastric cancer therapy. © 2011 Elsevier Ireland Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/148666
ISSN
0304-3835
2023 Impact Factor: 9.1
2023 SCImago Journal Rankings: 2.595
ISI Accession Number ID
WOS:000297895800008
Funding AgencyGrant Number
University of Hong Kong Research Committee200711159034
Funding Information:

The University of Hong Kong Research Committee Seed Funding Grant (Grant Code: 200711159034) provided the financial support for all necessary materials involved in this study.

References
References in Scopus
Grants
Interaction of XIAP and Jagged1 in colon cancer

 

DC FieldValueLanguage
dc.contributor.authorLi, Zen_HK
dc.contributor.authorChen, Jen_HK
dc.contributor.authorChan, KWen_HK
dc.contributor.authorQiao, Len_HK
dc.contributor.authorWong, BCYen_HK
dc.date.accessioned2012-05-29T06:14:32Z-
dc.date.available2012-05-29T06:14:32Z-
dc.date.issued2011en_HK
dc.identifier.citationCancer Letters, 2011, v. 313 n. 2, p. 192-200en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/148666-
dc.description.abstractCellular inhibitor of apoptosis protein 2 (cIAP2) is a member of the IAP family and is over-expressed in most cancer tissues. In this study, we investigated the role cIAP2 in Helicobacter pylori (HP) related gastric carcinogenesis. We measured the expression of cIAP2 at mRNA and protein levels in a panel of gastric cancer cell lines and human gastric cancer tissues by semi-quantitative reverse transcriptase PCR (RT-PCR), quantitative real time PCR (qPCR), immunoblotting, and immunohistochemistry. The effects of cIAP2 down-regulation on gastric cell proliferation and apoptosis were detected by standard WST-1 assay and flow cytometry, respectively. Infection of gastric mucosa by HP enhances the expression of cIAP2 in mouse gastric tissues. Over 70% of human gastric cancer tissues express higher amount of cIAP2. Well-differentiated gastric cancer cells express more cIAP2 than moderately- and poorly-differentiated gastric cancer cells. Knocking down of cIAP2 in SGC-7901 cells results in a 30% decrease in cell proliferation, a 20% increase in apoptosis and delayed migration. Thus, cIAP2 may play an important role in HP-induced gastric carcinogenesis, and it may serve as a potential target for gastric cancer therapy. © 2011 Elsevier Ireland Ltd.en_HK
dc.languageengen_US
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canleten_HK
dc.relation.ispartofCancer Lettersen_HK
dc.subjectCarcinogenesisen_HK
dc.subjectCIAP2en_HK
dc.subjectGastric canceren_HK
dc.subjectGene therapyen_HK
dc.subjectHelicobacter pylorien_HK
dc.subject.meshAnimalsen_US
dc.subject.meshApoptosis - Geneticsen_US
dc.subject.meshCell Line, Tumoren_US
dc.subject.meshCell Movement - Geneticsen_US
dc.subject.meshCell Proliferationen_US
dc.subject.meshDown-Regulationen_US
dc.subject.meshGastric Mucosa - Metabolism - Microbiologyen_US
dc.subject.meshHelicobacter Pylori - Pathogenicityen_US
dc.subject.meshHumansen_US
dc.subject.meshInhibitor Of Apoptosis Proteins - Genetics - Metabolismen_US
dc.subject.meshMaleen_US
dc.subject.meshMiceen_US
dc.subject.meshRna Interferenceen_US
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_US
dc.subject.meshStomach Neoplasms - Metabolism - Microbiology - Pathologyen_US
dc.titleA possible role of cIAP2 in Helicobacter pylori-associated gastric canceren_HK
dc.typeArticleen_HK
dc.identifier.emailChan, KW: hrmtckw@hku.hken_HK
dc.identifier.emailQiao, L: lq8688@hotmail.comen_HK
dc.identifier.emailWong, BCY: bcywong@hku.hken_HK
dc.identifier.authorityChan, KW=rp00330en_HK
dc.identifier.authorityQiao, L=rp00513en_HK
dc.identifier.authorityWong, BCY=rp00429en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1016/j.canlet.2011.09.007en_HK
dc.identifier.pmid21963223-
dc.identifier.scopuseid_2-s2.0-82655181796en_HK
dc.identifier.hkuros206234-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-82655181796&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume313en_HK
dc.identifier.issue2en_HK
dc.identifier.spage192en_HK
dc.identifier.epage200en_HK
dc.identifier.isiWOS:000297895800008-
dc.publisher.placeIrelanden_HK
dc.relation.projectInteraction of XIAP and Jagged1 in colon cancer-
dc.identifier.scopusauthoridLi, Z=37037717000en_HK
dc.identifier.scopusauthoridChen, J=22957233400en_HK
dc.identifier.scopusauthoridChan, KW=16444133100en_HK
dc.identifier.scopusauthoridQiao, L=7202151719en_HK
dc.identifier.scopusauthoridWong, BCY=7402023340en_HK
dc.identifier.citeulike9841075-
dc.identifier.issnl0304-3835-

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