File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Targeting cadherin-17 inactivates Wnt signaling and inhibits tumor growth in liver carcinoma
  • Basic View
  • Metadata View
  • XML View
TitleTargeting cadherin-17 inactivates Wnt signaling and inhibits tumor growth in liver carcinoma
 
AuthorsLiu, LX2 4
Lee, NP2
Chan, VW2
Xue, W1
Zender, L1
Zhang, C3
Mao, M3
Dai, H3
Wang, XL4
Xu, MZ2
Lee, TK2
Ng, IO2
Chen, Y5
Kung, HF5
Lowe, SW1
Poon, RTP2
Wang, JH4
Luk, JM2 6
 
Issue Date2009
 
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
 
CitationHepatology, 2009, v. 50 n. 5, p. 1453-1463 [How to Cite?]
DOI: http://dx.doi.org/10.1002/hep.23143
 
AbstractHepatocellular carcinoma (HCC) is a lethal malignancy for which there are no effective therapies. To develop rational therapeutic approaches for treating this disease, we are performing proof-of-principle studies targeting molecules crucial for the development of HCC. Here, we show that cadherin-17 (CDH17) adhesion molecule is up-regulated in human liver cancers and can transform premalignant liver progenitor cells to produce liver carcinomas in mice. RNA interference-mediated knockdown of CDH17 inhibited proliferation of both primary and highly metastatic HCC cell lines in vitro and in vivo. The antitumor mechanisms underlying CDH17 inhibition involve inactivation of Wnt signaling, because growth inhibition and cell death were accompanied by relocalization of β-catenin to the cytoplasm and a concomitant reduction in cyclin D1 and an increase in retinoblastoma. Conclusion: Our results identify CDH17 as a novel oncogene in HCC and suggest that CDH17 is a biomarker and attractive therapeutic target for this aggressive malignancy. Copyright © 2009 by the American Association for the Study of Liver Diseases.
 
ISSN0270-9139
2013 Impact Factor: 11.190
 
DOIhttp://dx.doi.org/10.1002/hep.23143
 
PubMed Central IDPMC3328302
 
ISI Accession Number IDWOS:000271565600017
Funding AgencyGrant Number
Research Grants Council of Hong KongHKU771607M
Collaborative Research FundHKU1/06C
National Cancer InstituteCA13106
Funding Information:

Supported by General Research Fund Grant HKU771607M from the Research Grants Council of Hong Kong (to J. M. L.). I. O. N. is Loke Yew Professor in Pathology and is supported by Collaborative Research Fund Grant HKU1/06C. S. W L. is a Howard Hughes Medical Institute investigator and is supported by National Cancer Institute Grant CA13106.

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLiu, LX
 
dc.contributor.authorLee, NP
 
dc.contributor.authorChan, VW
 
dc.contributor.authorXue, W
 
dc.contributor.authorZender, L
 
dc.contributor.authorZhang, C
 
dc.contributor.authorMao, M
 
dc.contributor.authorDai, H
 
dc.contributor.authorWang, XL
 
dc.contributor.authorXu, MZ
 
dc.contributor.authorLee, TK
 
dc.contributor.authorNg, IO
 
dc.contributor.authorChen, Y
 
dc.contributor.authorKung, HF
 
dc.contributor.authorLowe, SW
 
dc.contributor.authorPoon, RTP
 
dc.contributor.authorWang, JH
 
dc.contributor.authorLuk, JM
 
dc.date.accessioned2010-09-06T09:45:23Z
 
dc.date.available2010-09-06T09:45:23Z
 
dc.date.issued2009
 
dc.description.abstractHepatocellular carcinoma (HCC) is a lethal malignancy for which there are no effective therapies. To develop rational therapeutic approaches for treating this disease, we are performing proof-of-principle studies targeting molecules crucial for the development of HCC. Here, we show that cadherin-17 (CDH17) adhesion molecule is up-regulated in human liver cancers and can transform premalignant liver progenitor cells to produce liver carcinomas in mice. RNA interference-mediated knockdown of CDH17 inhibited proliferation of both primary and highly metastatic HCC cell lines in vitro and in vivo. The antitumor mechanisms underlying CDH17 inhibition involve inactivation of Wnt signaling, because growth inhibition and cell death were accompanied by relocalization of β-catenin to the cytoplasm and a concomitant reduction in cyclin D1 and an increase in retinoblastoma. Conclusion: Our results identify CDH17 as a novel oncogene in HCC and suggest that CDH17 is a biomarker and attractive therapeutic target for this aggressive malignancy. Copyright © 2009 by the American Association for the Study of Liver Diseases.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationHepatology, 2009, v. 50 n. 5, p. 1453-1463 [How to Cite?]
DOI: http://dx.doi.org/10.1002/hep.23143
 
dc.identifier.doihttp://dx.doi.org/10.1002/hep.23143
 
dc.identifier.eissn1527-3350
 
dc.identifier.epage1463
 
dc.identifier.hkuros168580
 
dc.identifier.isiWOS:000271565600017
Funding AgencyGrant Number
Research Grants Council of Hong KongHKU771607M
Collaborative Research FundHKU1/06C
National Cancer InstituteCA13106
Funding Information:

Supported by General Research Fund Grant HKU771607M from the Research Grants Council of Hong Kong (to J. M. L.). I. O. N. is Loke Yew Professor in Pathology and is supported by Collaborative Research Fund Grant HKU1/06C. S. W L. is a Howard Hughes Medical Institute investigator and is supported by National Cancer Institute Grant CA13106.

 
dc.identifier.issn0270-9139
2013 Impact Factor: 11.190
 
dc.identifier.issue5
 
dc.identifier.openurl
 
dc.identifier.pmcidPMC3328302
 
dc.identifier.pmid19676131
 
dc.identifier.scopuseid_2-s2.0-72949084408
 
dc.identifier.spage1453
 
dc.identifier.urihttp://hdl.handle.net/10722/88591
 
dc.identifier.volume50
 
dc.languageeng
 
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofHepatology
 
dc.relation.referencesReferences in Scopus
 
dc.rightsThe definitive version is available at www3.interscience.wiley.com
 
dc.subject.meshCadherins - genetics - metabolism
 
dc.subject.meshCarcinoma, Hepatocellular - metabolism - pathology
 
dc.subject.meshCell Proliferation
 
dc.subject.meshLiver Neoplasms - metabolism - pathology
 
dc.subject.meshSignal Transduction - physiology
 
dc.titleTargeting cadherin-17 inactivates Wnt signaling and inhibits tumor growth in liver carcinoma
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Liu, LX</contributor.author>
<contributor.author>Lee, NP</contributor.author>
<contributor.author>Chan, VW</contributor.author>
<contributor.author>Xue, W</contributor.author>
<contributor.author>Zender, L</contributor.author>
<contributor.author>Zhang, C</contributor.author>
<contributor.author>Mao, M</contributor.author>
<contributor.author>Dai, H</contributor.author>
<contributor.author>Wang, XL</contributor.author>
<contributor.author>Xu, MZ</contributor.author>
<contributor.author>Lee, TK</contributor.author>
<contributor.author>Ng, IO</contributor.author>
<contributor.author>Chen, Y</contributor.author>
<contributor.author>Kung, HF</contributor.author>
<contributor.author>Lowe, SW</contributor.author>
<contributor.author>Poon, RTP</contributor.author>
<contributor.author>Wang, JH</contributor.author>
<contributor.author>Luk, JM</contributor.author>
<date.accessioned>2010-09-06T09:45:23Z</date.accessioned>
<date.available>2010-09-06T09:45:23Z</date.available>
<date.issued>2009</date.issued>
<identifier.citation>Hepatology, 2009, v. 50 n. 5, p. 1453-1463</identifier.citation>
<identifier.issn>0270-9139</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/88591</identifier.uri>
<description.abstract>Hepatocellular carcinoma (HCC) is a lethal malignancy for which there are no effective therapies. To develop rational therapeutic approaches for treating this disease, we are performing proof-of-principle studies targeting molecules crucial for the development of HCC. Here, we show that cadherin-17 (CDH17) adhesion molecule is up-regulated in human liver cancers and can transform premalignant liver progenitor cells to produce liver carcinomas in mice. RNA interference-mediated knockdown of CDH17 inhibited proliferation of both primary and highly metastatic HCC cell lines in vitro and in vivo. The antitumor mechanisms underlying CDH17 inhibition involve inactivation of Wnt signaling, because growth inhibition and cell death were accompanied by relocalization of &#946;-catenin to the cytoplasm and a concomitant reduction in cyclin D1 and an increase in retinoblastoma. Conclusion: Our results identify CDH17 as a novel oncogene in HCC and suggest that CDH17 is a biomarker and attractive therapeutic target for this aggressive malignancy. Copyright &#169; 2009 by the American Association for the Study of Liver Diseases.</description.abstract>
<language>eng</language>
<publisher>John Wiley &amp; Sons, Inc. The Journal&apos;s web site is located at http://www.hepatology.org/</publisher>
<relation.ispartof>Hepatology</relation.ispartof>
<rights>The definitive version is available at www3.interscience.wiley.com</rights>
<subject.mesh>Cadherins - genetics - metabolism</subject.mesh>
<subject.mesh>Carcinoma, Hepatocellular - metabolism - pathology</subject.mesh>
<subject.mesh>Cell Proliferation</subject.mesh>
<subject.mesh>Liver Neoplasms - metabolism - pathology</subject.mesh>
<subject.mesh>Signal Transduction - physiology</subject.mesh>
<title>Targeting cadherin-17 inactivates Wnt signaling and inhibits tumor growth in liver carcinoma</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=0270-9139&amp;volume=50&amp;issue=5&amp;spage=1453&amp;epage=1463&amp;date=2009&amp;atitle=Targeting+cadherin-17+inactivates+Wnt+signaling+and+inhibits+tumor+growth+in+liver+carcinoma</identifier.openurl>
<description.nature>Link_to_subscribed_fulltext</description.nature>
<identifier.doi>10.1002/hep.23143</identifier.doi>
<identifier.pmid>19676131</identifier.pmid>
<identifier.pmcid>PMC3328302</identifier.pmcid>
<identifier.scopus>eid_2-s2.0-72949084408</identifier.scopus>
<identifier.hkuros>168580</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-72949084408&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>50</identifier.volume>
<identifier.issue>5</identifier.issue>
<identifier.spage>1453</identifier.spage>
<identifier.epage>1463</identifier.epage>
<identifier.eissn>1527-3350</identifier.eissn>
<identifier.isi>WOS:000271565600017</identifier.isi>
<publisher.place>United States</publisher.place>
</item>
Author Affiliations
  1. Howard Hughes Medical Institute
  2. The University of Hong Kong
  3. Rosetta Inpharmatics LLC
  4. Fudan University
  5. Chinese University of Hong Kong
  6. Pfizer