File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Granulin-epithelin precursor as a therapeutic target for hepatocellular carcinoma

TitleGranulin-epithelin precursor as a therapeutic target for hepatocellular carcinoma
Authors
Issue Date2008
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/
Citation
Hepatology, 2008, v. 47 n. 5, p. 1524-1532 How to Cite?
AbstractPrimary liver cancer, hepatocellular carcinoma (HCC), is the fifth most common cancer and the third leading cancer killer in the world. There is no effective therapeutic option for most HCC patients. A new therapeutic strategy is essential. Granulin-epithelin precursor (GEP, also called progranulin, acrogranin, or PC-derived growth factor) was identified as a potential therapeutic target for HCC from our earlier genome-wide expression profiles. We aimed to conduct a detailed investigation with in vitro and animal experiments. We developed the anti-GEP monoclonal antibody (mAb), and examined its effect on hepatoma cells and normal liver cells in vitro. A nude mice model transplanted with human HCC was used to investigate if anti-GEP mAb can inhibit tumor growth in vivo. We demonstrated that anti-GEP mAb inhibited the growth of hepatoma cells but revealed no significant effect on normal liver cells. In the nude mice model transplanted with human HCC, anti-GEP mAb decreased the serum GEP level and inhibited the growth of established tumors in a dose-dependent manner. The anti-GEP mAb reduced tumor cell proliferation via the p44/42 MAPK and Akt pathways, and reduced tumor angiogenesis to deprive the nutrient supply with reduced microvessel density and tumor vascular endothelial growth factor level. Conclusion: We have shown that anti-GEP antibody can inhibit HCC growth, providing evidence that GEP is a therapeutic target for HCC treatment. Copyright © 2008 by the American Association for the Study of Liver Diseases.
Persistent Identifierhttp://hdl.handle.net/10722/84086
ISSN
2015 Impact Factor: 11.711
2015 SCImago Journal Rankings: 4.752
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHo, JCen_HK
dc.contributor.authorIp, YCen_HK
dc.contributor.authorCheung, STen_HK
dc.contributor.authorLee, YTen_HK
dc.contributor.authorChan, KFen_HK
dc.contributor.authorWong, SYen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T08:48:46Z-
dc.date.available2010-09-06T08:48:46Z-
dc.date.issued2008en_HK
dc.identifier.citationHepatology, 2008, v. 47 n. 5, p. 1524-1532en_HK
dc.identifier.issn0270-9139en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84086-
dc.description.abstractPrimary liver cancer, hepatocellular carcinoma (HCC), is the fifth most common cancer and the third leading cancer killer in the world. There is no effective therapeutic option for most HCC patients. A new therapeutic strategy is essential. Granulin-epithelin precursor (GEP, also called progranulin, acrogranin, or PC-derived growth factor) was identified as a potential therapeutic target for HCC from our earlier genome-wide expression profiles. We aimed to conduct a detailed investigation with in vitro and animal experiments. We developed the anti-GEP monoclonal antibody (mAb), and examined its effect on hepatoma cells and normal liver cells in vitro. A nude mice model transplanted with human HCC was used to investigate if anti-GEP mAb can inhibit tumor growth in vivo. We demonstrated that anti-GEP mAb inhibited the growth of hepatoma cells but revealed no significant effect on normal liver cells. In the nude mice model transplanted with human HCC, anti-GEP mAb decreased the serum GEP level and inhibited the growth of established tumors in a dose-dependent manner. The anti-GEP mAb reduced tumor cell proliferation via the p44/42 MAPK and Akt pathways, and reduced tumor angiogenesis to deprive the nutrient supply with reduced microvessel density and tumor vascular endothelial growth factor level. Conclusion: We have shown that anti-GEP antibody can inhibit HCC growth, providing evidence that GEP is a therapeutic target for HCC treatment. Copyright © 2008 by the American Association for the Study of Liver Diseases.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.hepatology.org/en_HK
dc.relation.ispartofHepatologyen_HK
dc.rightsHepatology. Copyright © John Wiley & Sons, Inc.en_HK
dc.titleGranulin-epithelin precursor as a therapeutic target for hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-9139&volume=47&spage=1524&epage=1532&date=2008&atitle=Granulin-epithelin+precursor+as+a+therapeutic+target+for+hepatocellular+carcinomaen_HK
dc.identifier.emailSiu, TC: stcheung@hkucc.hku.hken_HK
dc.identifier.authoritySiu, TC=rp00457en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/hep.22191en_HK
dc.identifier.pmid18393387-
dc.identifier.scopuseid_2-s2.0-43949142502en_HK
dc.identifier.hkuros141631en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-43949142502&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume47en_HK
dc.identifier.issue5en_HK
dc.identifier.spage1524en_HK
dc.identifier.epage1532en_HK
dc.identifier.eissn1527-3350-
dc.identifier.isiWOS:000255507500012-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHo, JC=7402650173en_HK
dc.identifier.scopusauthoridYing, CI=14039827000en_HK
dc.identifier.scopusauthoridSiu, TC=7202473497en_HK
dc.identifier.scopusauthoridYuk, TL=14632582400en_HK
dc.identifier.scopusauthoridKui, FC=24281425500en_HK
dc.identifier.scopusauthoridSan, YW=36780044200en_HK
dc.identifier.scopusauthoridSheung, TF=6506234707en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats