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- Publisher Website: 10.1002/hep.23143
- Scopus: eid_2-s2.0-72949084408
- PMID: 19676131
- WOS: WOS:000271565600017
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Article: Targeting cadherin-17 inactivates Wnt signaling and inhibits tumor growth in liver carcinoma
Title | Targeting cadherin-17 inactivates Wnt signaling and inhibits tumor growth in liver carcinoma | ||||||||
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Authors | |||||||||
Issue Date | 2009 | ||||||||
Publisher | John Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/ | ||||||||
Citation | Hepatology, 2009, v. 50 n. 5, p. 1453-1463 How to Cite? | ||||||||
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 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. | ||||||||
Persistent Identifier | http://hdl.handle.net/10722/88591 | ||||||||
ISSN | 2023 Impact Factor: 12.9 2023 SCImago Journal Rankings: 5.011 | ||||||||
PubMed Central ID | |||||||||
ISI Accession Number ID |
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. | ||||||||
References |
DC Field | Value | Language |
---|---|---|
dc.contributor.author | Liu, LX | en_HK |
dc.contributor.author | Lee, NP | en_HK |
dc.contributor.author | Chan, VW | en_HK |
dc.contributor.author | Xue, W | en_HK |
dc.contributor.author | Zender, L | en_HK |
dc.contributor.author | Zhang, C | en_HK |
dc.contributor.author | Mao, M | en_HK |
dc.contributor.author | Dai, H | en_HK |
dc.contributor.author | Wang, XL | en_HK |
dc.contributor.author | Xu, MZ | en_HK |
dc.contributor.author | Lee, TK | en_HK |
dc.contributor.author | Ng, IO | en_HK |
dc.contributor.author | Chen, Y | en_HK |
dc.contributor.author | Kung, HF | en_HK |
dc.contributor.author | Lowe, SW | en_HK |
dc.contributor.author | Poon, RTP | en_HK |
dc.contributor.author | Wang, JH | en_HK |
dc.contributor.author | Luk, JM | en_HK |
dc.date.accessioned | 2010-09-06T09:45:23Z | - |
dc.date.available | 2010-09-06T09:45:23Z | - |
dc.date.issued | 2009 | en_HK |
dc.identifier.citation | Hepatology, 2009, v. 50 n. 5, p. 1453-1463 | en_HK |
dc.identifier.issn | 0270-9139 | en_HK |
dc.identifier.uri | http://hdl.handle.net/10722/88591 | - |
dc.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 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. | en_HK |
dc.language | eng | en_HK |
dc.publisher | John Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/ | en_HK |
dc.relation.ispartof | Hepatology | en_HK |
dc.rights | The definitive version is available at www3.interscience.wiley.com | en_HK |
dc.subject.mesh | Cadherins - genetics - metabolism | - |
dc.subject.mesh | Carcinoma, Hepatocellular - metabolism - pathology | - |
dc.subject.mesh | Cell Proliferation | - |
dc.subject.mesh | Liver Neoplasms - metabolism - pathology | - |
dc.subject.mesh | Signal Transduction - physiology | - |
dc.title | Targeting cadherin-17 inactivates Wnt signaling and inhibits tumor growth in liver carcinoma | en_HK |
dc.type | Article | en_HK |
dc.identifier.openurl | http://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-9139&volume=50&issue=5&spage=1453&epage=1463&date=2009&atitle=Targeting+cadherin-17+inactivates+Wnt+signaling+and+inhibits+tumor+growth+in+liver+carcinoma | en_HK |
dc.identifier.email | Lee, NP: nikkilee@hku.hk | en_HK |
dc.identifier.email | Lee, TK: tkwlee@hkucc.hku.hk | en_HK |
dc.identifier.email | Ng, IO: iolng@hkucc.hku.hk | en_HK |
dc.identifier.email | Poon, RTP: poontp@hkucc.hku.hk | en_HK |
dc.identifier.email | Luk, JM: jmluk@hkucc.hku.hk | en_HK |
dc.identifier.authority | Lee, NP=rp00263 | en_HK |
dc.identifier.authority | Lee, TK=rp00447 | en_HK |
dc.identifier.authority | Ng, IO=rp00335 | en_HK |
dc.identifier.authority | Poon, RTP=rp00446 | en_HK |
dc.identifier.authority | Luk, JM=rp00349 | en_HK |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1002/hep.23143 | en_HK |
dc.identifier.pmid | 19676131 | - |
dc.identifier.pmcid | PMC3328302 | - |
dc.identifier.scopus | eid_2-s2.0-72949084408 | en_HK |
dc.identifier.hkuros | 168580 | en_HK |
dc.relation.references | http://www.scopus.com/mlt/select.url?eid=2-s2.0-72949084408&selection=ref&src=s&origin=recordpage | en_HK |
dc.identifier.volume | 50 | en_HK |
dc.identifier.issue | 5 | en_HK |
dc.identifier.spage | 1453 | en_HK |
dc.identifier.epage | 1463 | en_HK |
dc.identifier.eissn | 1527-3350 | - |
dc.identifier.isi | WOS:000271565600017 | - |
dc.publisher.place | United States | en_HK |
dc.identifier.scopusauthorid | Liu, LX=13611939300 | en_HK |
dc.identifier.scopusauthorid | Lee, NP=7402722690 | en_HK |
dc.identifier.scopusauthorid | Chan, VW=36005663800 | en_HK |
dc.identifier.scopusauthorid | Xue, W=32267773000 | en_HK |
dc.identifier.scopusauthorid | Zender, L=6603035987 | en_HK |
dc.identifier.scopusauthorid | Zhang, C=7405492903 | en_HK |
dc.identifier.scopusauthorid | Mao, M=7102960472 | en_HK |
dc.identifier.scopusauthorid | Dai, H=7402206916 | en_HK |
dc.identifier.scopusauthorid | Wang, XL=9733112300 | en_HK |
dc.identifier.scopusauthorid | Xu, MZ=24339881700 | en_HK |
dc.identifier.scopusauthorid | Lee, TK=7501439435 | en_HK |
dc.identifier.scopusauthorid | Ng, IO=7102753722 | en_HK |
dc.identifier.scopusauthorid | Chen, Y=24075600300 | en_HK |
dc.identifier.scopusauthorid | Kung, HF=7402514190 | en_HK |
dc.identifier.scopusauthorid | Lowe, SW=15064198100 | en_HK |
dc.identifier.scopusauthorid | Poon, RTP=7103097223 | en_HK |
dc.identifier.scopusauthorid | Wang, JH=8898010700 | en_HK |
dc.identifier.scopusauthorid | Luk, JM=7006777791 | en_HK |
dc.identifier.issnl | 0270-9139 | - |