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Article: Id-1 promotes proliferation of p53-deficient esophageal cancer cells

TitleId-1 promotes proliferation of p53-deficient esophageal cancer cells
Authors
Issue Date2006
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, 2006, v. 119 n. 3, p. 508-514 How to Cite?
AbstractThe helix-loop-helix protein inhibitor of differentiation and DNA binding (Id-1) is known to promote cellular proliferation in several types of human cancer. Although it has been reported that Id-1 is over-expressed in esophageal squamous cell carcinoma (ESCC), its function and signaling pathways in esophageal cancer are unknown. In our study, we investigated the direct effects of Id-1 on esophageal cancer cell growth by transfecting an Id-1 expression vector into an ESCC cell line (HKESC-3), which showed serum-dependent Id-1 expression. Ectopic Id-1 expression resulted in increased serum-independent cell growth and G1-S phase transition, as well as up-regulation of mouse double minute 2 (MDM2) and down-regulation of p21Waf1/Cip1 protein expressions in the transfectant clones in a p53-independent manner. However, overexpression of Id-1 had no effect on the pRB, CDK4 and p16INK4A expressions. Stable transfection of Id-1 antisense expression vector to inhibit the expression of endogenous Id-1 in another ESCC cell line (HKESC-1) reversed the effects on MDM2 and p21Waf1/Cip1. In addition, Id-1 expression protected ESCC cells from Tumor Necrosis Factor (TNF)-α-induced apoptosis by up-regulating and activating Bcl-2. In conclusion, our study provides evidence for the first time that Id-1 plays a role in both proliferation and survival of esophageal cancer cells. Our findings also suggest that unlike prostate, hepatocellular and nasopharyngeal carcinomas in which Id-1 induces cell proliferation through inactivation of p16INK4A/RB pathway, the increased cell proliferation observed in ESCC cells may be mediated through a different mechanism. © 2006 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/67808
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHui, CMen_HK
dc.contributor.authorCheung, PYen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorCheung, ALMen_HK
dc.date.accessioned2010-09-06T05:58:26Z-
dc.date.available2010-09-06T05:58:26Z-
dc.date.issued2006en_HK
dc.identifier.citationInternational Journal Of Cancer, 2006, v. 119 n. 3, p. 508-514en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67808-
dc.description.abstractThe helix-loop-helix protein inhibitor of differentiation and DNA binding (Id-1) is known to promote cellular proliferation in several types of human cancer. Although it has been reported that Id-1 is over-expressed in esophageal squamous cell carcinoma (ESCC), its function and signaling pathways in esophageal cancer are unknown. In our study, we investigated the direct effects of Id-1 on esophageal cancer cell growth by transfecting an Id-1 expression vector into an ESCC cell line (HKESC-3), which showed serum-dependent Id-1 expression. Ectopic Id-1 expression resulted in increased serum-independent cell growth and G1-S phase transition, as well as up-regulation of mouse double minute 2 (MDM2) and down-regulation of p21Waf1/Cip1 protein expressions in the transfectant clones in a p53-independent manner. However, overexpression of Id-1 had no effect on the pRB, CDK4 and p16INK4A expressions. Stable transfection of Id-1 antisense expression vector to inhibit the expression of endogenous Id-1 in another ESCC cell line (HKESC-1) reversed the effects on MDM2 and p21Waf1/Cip1. In addition, Id-1 expression protected ESCC cells from Tumor Necrosis Factor (TNF)-α-induced apoptosis by up-regulating and activating Bcl-2. In conclusion, our study provides evidence for the first time that Id-1 plays a role in both proliferation and survival of esophageal cancer cells. Our findings also suggest that unlike prostate, hepatocellular and nasopharyngeal carcinomas in which Id-1 induces cell proliferation through inactivation of p16INK4A/RB pathway, the increased cell proliferation observed in ESCC cells may be mediated through a different mechanism. © 2006 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.meshBlotting, Westernen_HK
dc.subject.meshCarcinoma, Squamous Cell - genetics - metabolism - pathologyen_HK
dc.subject.meshCell Cycle - physiologyen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshCell Survival - physiologyen_HK
dc.subject.meshCulture Media - pharmacologyen_HK
dc.subject.meshCulture Media, Serum-Free - pharmacologyen_HK
dc.subject.meshCyclin-Dependent Kinase Inhibitor p16 - metabolismen_HK
dc.subject.meshCyclin-Dependent Kinase Inhibitor p21 - metabolismen_HK
dc.subject.meshDNA, Antisense - geneticsen_HK
dc.subject.meshEsophageal Neoplasms - genetics - metabolism - pathologyen_HK
dc.subject.meshGene Expression - drug effectsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInhibitor of Differentiation Protein 1 - genetics - metabolism - physiologyen_HK
dc.subject.meshProto-Oncogene Proteins c-mdm2 - metabolismen_HK
dc.subject.meshRetinoblastoma Protein - metabolismen_HK
dc.subject.meshSignal Transduction - physiologyen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshTumor Suppressor Protein p53 - deficiency - metabolismen_HK
dc.titleId-1 promotes proliferation of p53-deficient esophageal cancer cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0020-7136&volume=119&spage=508&epage=514&date=2006&atitle=Id-1+promotes+proliferation+of+p53-deficient+esophageal+cancer+cellsen_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.emailCheung, ALM:lmcheung@hkucc.hku.hken_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.21874en_HK
dc.identifier.pmid16506209-
dc.identifier.scopuseid_2-s2.0-33745475219en_HK
dc.identifier.hkuros115760en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33745475219&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume119en_HK
dc.identifier.issue3en_HK
dc.identifier.spage508en_HK
dc.identifier.epage514en_HK
dc.identifier.isiWOS:000238476800005-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHui, CM=14024315600en_HK
dc.identifier.scopusauthoridCheung, PY=14024149900en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK

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