File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
  • Find via Find It@HKUL
Supplementary

Conference Paper: Id-1 activation of PI3K/Akt signaling pathway and its significance in promoting tumorigenicity and metastasis of human esophageal cancer cells

TitleId-1 activation of PI3K/Akt signaling pathway and its significance in promoting tumorigenicity and metastasis of human esophageal cancer cells
Authors
Issue Date2009
PublisherAmerican Association for Cancer Research
Citation
The 100th AACR Annual Meeting, Denver, CO., 18-22 April 2009. In Cancer Research, 2009, v. 69 n. 9S, p. 4348 How to Cite?
AbstractId-1 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 PI3K/Akt signaling pathway in human esophageal cancer cells. In this study, we confirmed a positive correlation between Id-1 expression and phospho-Akt in ESCC cell lines, as well as in ESCC tumor tissues from patients. To investigate the significance of Id-1 in esophageal cancer progression, we also conducted in vivo experiments to compare the tumorigenic and metastatic potential of an Id-1-overexpressing ESCC cell line in nude mice with that of the control cell line expressing the empty vector. We found that the Id-1 overexpressing cancer cells produced significantly larger tumors when inoculated subcutaneously into the flank of nude mice, and pronounced lung metastasis when injected intravenously into the tail vein. The tumor xenografts of esophageal cancer cells with stable ectopic Id-1 expression showed elevated Ki-67 proliferation index and increased angiogenesis, as well as reduced apoptosis. 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 (EMT), 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 (MMP-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. [This study is supported by The University of Hong Kong CRCG Small Project Funding Programme (Project No. 200807176012) and by a Collaborative Research Fund from the Research Grants Council of the Hong Kong Special Administrative Region, China (Project No. HKUST2/06C)]
Persistent Identifierhttp://hdl.handle.net/10722/61395
ISSN
2015 Impact Factor: 8.556
2015 SCImago Journal Rankings: 5.372

 

DC FieldValueLanguage
dc.contributor.authorCheung, Aen_HK
dc.contributor.authorLi, Ben_HK
dc.contributor.authorTsao, GSWen_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.date.accessioned2010-07-13T03:38:48Z-
dc.date.available2010-07-13T03:38:48Z-
dc.date.issued2009en_HK
dc.identifier.citationThe 100th AACR Annual Meeting, Denver, CO., 18-22 April 2009. In Cancer Research, 2009, v. 69 n. 9S, p. 4348en_HK
dc.identifier.issn0008-5472-
dc.identifier.urihttp://hdl.handle.net/10722/61395-
dc.description.abstractId-1 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 PI3K/Akt signaling pathway in human esophageal cancer cells. In this study, we confirmed a positive correlation between Id-1 expression and phospho-Akt in ESCC cell lines, as well as in ESCC tumor tissues from patients. To investigate the significance of Id-1 in esophageal cancer progression, we also conducted in vivo experiments to compare the tumorigenic and metastatic potential of an Id-1-overexpressing ESCC cell line in nude mice with that of the control cell line expressing the empty vector. We found that the Id-1 overexpressing cancer cells produced significantly larger tumors when inoculated subcutaneously into the flank of nude mice, and pronounced lung metastasis when injected intravenously into the tail vein. The tumor xenografts of esophageal cancer cells with stable ectopic Id-1 expression showed elevated Ki-67 proliferation index and increased angiogenesis, as well as reduced apoptosis. 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 (EMT), 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 (MMP-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. [This study is supported by The University of Hong Kong CRCG Small Project Funding Programme (Project No. 200807176012) and by a Collaborative Research Fund from the Research Grants Council of the Hong Kong Special Administrative Region, China (Project No. HKUST2/06C)]-
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research-
dc.relation.ispartofCancer Research-
dc.titleId-1 activation of PI3K/Akt signaling pathway and its significance in promoting tumorigenicity and metastasis of human esophageal cancer cellsen_HK
dc.typeConference_Paperen_HK
dc.identifier.emailCheung, A: lmcheung@hkucc.hku.hken_HK
dc.identifier.emailTsao, GSW: gswtsao@hkucc.hku.hken_HK
dc.identifier.emailLi, YY: yyli@HKUCC.hku.hken_HK
dc.identifier.emailWang, X: xhwang@HKUCC.hku.hken_HK
dc.identifier.emailLing, MT: patling@HKUCC.hku.hken_HK
dc.identifier.emailWong, YC: ycwong@hkucc.hku.hken_HK
dc.identifier.authorityCheung, A=rp00332en_HK
dc.identifier.authorityTsao, GSW=rp00399en_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.identifier.hkuros155392en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats