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Article: Id-1 promotes tumorigenicity and metastasis of human esophageal cancer cells through activation of PI3K/AKT signaling pathway

TitleId-1 promotes tumorigenicity and metastasis of human esophageal cancer cells through activation of PI3K/AKT signaling pathway
Authors
Issue Date2009
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, 2009, v. 125 n. 11, p. 2576-2585 How to Cite?
AbstractId-1 (inhibitor of differentiation or DNA binding) is a helix-loop-helix protein that is overexpressed in many types of cancer including esophageal squamous cell carcinoma (ESCC). We previously reported that ectopic Id-1 expression activates the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway in human esophageal cancer cells. In this study, we confirmed a positive correlation between Id-1 and phospho-AKT (Ser473) expressions in ESCC cell lines, as well as in ESCC on a tissue microarray. To investigate the significance of Id-1 in esophageal cancer progression, ESCC cells with stable ectopic Id-1 expression were inoculated subcutaneously into the flank of nude mice and were found to form larger tumors that showed elevated Ki-67 proliferation index and increased angiogenesis, as well as reduced apoptosis, compared with control cells expressing the empty vector. The Id-1-overexpressing cells also exhibited enhanced metastatic potential in the experimental metastasis assay. Treatment with the PI3K inhibitor LY294002 attenuated the tumor promotion effects of Id-1, indicating that the effects were mediated by the PI3K/AKT signaling pathway. In addition, our in vitro experiments showed that ectopic Id-1 expression altered the expression levels of markers associated with epithelial-mesenchymal transition and enhanced the migration ability of esophageal cancer cells. The Id-1-overexpressing ESCC cells also exhibited increased invasive potential, which was in part due to PI3K/AKT-dependent modulation of matrix metalloproteinase-9 expression. In conclusion, our results provide the first evidence that Id-1 promotes tumorigenicity and metastasis of human esophageal cancer in vivo and that the PI3K inhibitor LY294002 can attenuate these effects. © 2009 UICC.
Persistent Identifierhttp://hdl.handle.net/10722/58228
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
Funding AgencyGrant Number
University of Hong Kong CRCG Small Project Funding Programme20067176143
20087176012
Hong Kong Special Administrative Region, ChinaHKUST 2/06C
Funding Information:

Grant sponsor: University of Hong Kong CRCG Small Project Funding Programme; Grant numbers: 20067176143 and 20087176012; Research Grants Council of the Hong Kong Special Administrative Region, China, Collaborative Research Fund; Grant number: HKUST 2/06C.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorLi, Ben_HK
dc.contributor.authorTsao, SWen_HK
dc.contributor.authorLi, YYen_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorWong, YCen_HK
dc.contributor.authorHe, QYen_HK
dc.contributor.authorCheung, ALMen_HK
dc.date.accessioned2010-05-31T03:26:13Z-
dc.date.available2010-05-31T03:26:13Z-
dc.date.issued2009en_HK
dc.identifier.citationInternational Journal Of Cancer, 2009, v. 125 n. 11, p. 2576-2585en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/58228-
dc.description.abstractId-1 (inhibitor of differentiation or DNA binding) is a helix-loop-helix protein that is overexpressed in many types of cancer including esophageal squamous cell carcinoma (ESCC). We previously reported that ectopic Id-1 expression activates the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (AKT) signaling pathway in human esophageal cancer cells. In this study, we confirmed a positive correlation between Id-1 and phospho-AKT (Ser473) expressions in ESCC cell lines, as well as in ESCC on a tissue microarray. To investigate the significance of Id-1 in esophageal cancer progression, ESCC cells with stable ectopic Id-1 expression were inoculated subcutaneously into the flank of nude mice and were found to form larger tumors that showed elevated Ki-67 proliferation index and increased angiogenesis, as well as reduced apoptosis, compared with control cells expressing the empty vector. The Id-1-overexpressing cells also exhibited enhanced metastatic potential in the experimental metastasis assay. Treatment with the PI3K inhibitor LY294002 attenuated the tumor promotion effects of Id-1, indicating that the effects were mediated by the PI3K/AKT signaling pathway. In addition, our in vitro experiments showed that ectopic Id-1 expression altered the expression levels of markers associated with epithelial-mesenchymal transition and enhanced the migration ability of esophageal cancer cells. The Id-1-overexpressing ESCC cells also exhibited increased invasive potential, which was in part due to PI3K/AKT-dependent modulation of matrix metalloproteinase-9 expression. In conclusion, our results provide the first evidence that Id-1 promotes tumorigenicity and metastasis of human esophageal cancer in vivo and that the PI3K inhibitor LY294002 can attenuate these effects. © 2009 UICC.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.meshAnimalsen_HK
dc.subject.meshApoptosisen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshCarcinoma, Squamous Cell - metabolism - pathologyen_HK
dc.subject.meshCell Movementen_HK
dc.subject.meshCell Proliferationen_HK
dc.subject.meshEsophageal Neoplasms - metabolism - pathologyen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshFluorescent Antibody Techniqueen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunoenzyme Techniquesen_HK
dc.subject.meshInhibitor of Differentiation Protein 1 - physiologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred BALB Cen_HK
dc.subject.meshMice, Nudeen_HK
dc.subject.meshNeoplasm Invasivenessen_HK
dc.subject.meshPhosphatidylinositol 3-Kinases - metabolismen_HK
dc.subject.meshProto-Oncogene Proteins c-akt - metabolismen_HK
dc.subject.meshSignal Transductionen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.subject.meshWound Healingen_HK
dc.subject.meshXenograft Model Antitumor Assaysen_HK
dc.titleId-1 promotes tumorigenicity and metastasis of human esophageal cancer cells through activation of PI3K/AKT signaling pathwayen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0020-7136&volume=125&spage=2576&epage=2585&date=2009&atitle=Id-1+promotes+tumorigenicity+and+metastasis+of+human+esophageal+cancer+cells+through+activation+of+PI3K/AKT+signaling+pathwayen_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.emailLing, MT:patling@hkucc.hku.hken_HK
dc.identifier.emailWong, YC:ycwong@hkucc.hku.hken_HK
dc.identifier.emailCheung, ALM:lmcheung@hkucc.hku.hken_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.24675en_HK
dc.identifier.pmid19551863en_HK
dc.identifier.scopuseid_2-s2.0-70350704818en_HK
dc.identifier.hkuros167804en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-70350704818&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume125en_HK
dc.identifier.issue11en_HK
dc.identifier.spage2576en_HK
dc.identifier.epage2585en_HK
dc.identifier.isiWOS:000271516500011-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.relation.projectEsophageal Carcinoma Research Center-
dc.identifier.scopusauthoridLi, B=16138329900en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK
dc.identifier.scopusauthoridLi, YY=8293496300en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK
dc.identifier.scopusauthoridHe, QY=34770287900en_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK

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