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Article: Hedgehog signaling in human hepatocellular carcinoma

TitleHedgehog signaling in human hepatocellular carcinoma
Authors
KeywordsCyclopamine
HCC
Hedgehog
Issue Date2006
PublisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cbt/index.php
Citation
Cancer Biology And Therapy, 2006, v. 5 n. 1, p. 111-117 How to Cite?
AbstractHepatocellular carcinoma (HCC) is the fourth most common malignancy and one of the leading causes of death world wide. Signaling pathways important for tumor initiation and progression in HCC are poorly understood. Hedgehog signaling (Hh) has been implicated in multiple events during development and has also been proposed to play important roles in several tumor types. However, it remains unclear whether this pathway is activated in HCC. Here, we report the detection of transcripts for hedgehog pathway signaling molecules in both HCC cell lines and tumor samples. Quantitative real-time RT-PCR also revealed the decreased expression of Hip1 and increased expression of Gli 1 and smo in HCC samples compared with nontumor liver tissues. Blocking the hedgehog pathway with cyclopamine inhibited proliferation, induced apoptosis and repressed c-Myc and cyclin D expression in a subset of HCC cell lines. The study therefore, for the first time, provides evidence that hedgehog signaling may be activated in some HCC tumors. The results also indicate that the hedgehog pathway may be a new candidate for therapeutic targeting in HCC. ©2005 Landes Bioscience.
Persistent Identifierhttp://hdl.handle.net/10722/84409
ISSN
2015 Impact Factor: 2.921
2015 SCImago Journal Rankings: 1.297
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorPatil, MAen_HK
dc.contributor.authorZhang, Jen_HK
dc.contributor.authorHo, Cen_HK
dc.contributor.authorCheung, STen_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorChen, Xen_HK
dc.date.accessioned2010-09-06T08:52:38Z-
dc.date.available2010-09-06T08:52:38Z-
dc.date.issued2006en_HK
dc.identifier.citationCancer Biology And Therapy, 2006, v. 5 n. 1, p. 111-117en_HK
dc.identifier.issn1538-4047en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84409-
dc.description.abstractHepatocellular carcinoma (HCC) is the fourth most common malignancy and one of the leading causes of death world wide. Signaling pathways important for tumor initiation and progression in HCC are poorly understood. Hedgehog signaling (Hh) has been implicated in multiple events during development and has also been proposed to play important roles in several tumor types. However, it remains unclear whether this pathway is activated in HCC. Here, we report the detection of transcripts for hedgehog pathway signaling molecules in both HCC cell lines and tumor samples. Quantitative real-time RT-PCR also revealed the decreased expression of Hip1 and increased expression of Gli 1 and smo in HCC samples compared with nontumor liver tissues. Blocking the hedgehog pathway with cyclopamine inhibited proliferation, induced apoptosis and repressed c-Myc and cyclin D expression in a subset of HCC cell lines. The study therefore, for the first time, provides evidence that hedgehog signaling may be activated in some HCC tumors. The results also indicate that the hedgehog pathway may be a new candidate for therapeutic targeting in HCC. ©2005 Landes Bioscience.en_HK
dc.languageengen_HK
dc.publisherLandes Bioscience. The Journal's web site is located at http://www.landesbioscience.com/journals/cbt/index.phpen_HK
dc.relation.ispartofCancer Biology and Therapyen_HK
dc.subjectCyclopamineen_HK
dc.subjectHCCen_HK
dc.subjectHedgehogen_HK
dc.titleHedgehog signaling in human hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1538-4047&volume=5&issue=1&spage=111&epage=117&date=2006&atitle=Hedgehog+signaling+in+human+hepatocellular+carcinomaen_HK
dc.identifier.emailCheung, ST: stcheung@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityCheung, ST=rp00457en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.pmid16397407-
dc.identifier.scopuseid_2-s2.0-32544437230en_HK
dc.identifier.hkuros116887en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-32544437230&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume5en_HK
dc.identifier.issue1en_HK
dc.identifier.spage111en_HK
dc.identifier.epage117en_HK
dc.identifier.isiWOS:000236044500026-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridPatil, MA=8559878100en_HK
dc.identifier.scopusauthoridZhang, J=9333032100en_HK
dc.identifier.scopusauthoridHo, C=8914892800en_HK
dc.identifier.scopusauthoridCheung, ST=7202473497en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.scopusauthoridChen, X=8978110800en_HK

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