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Article: Gold(III) compound is a novel chemocytotoxic agent for hepatocellular carcinoma

TitleGold(III) compound is a novel chemocytotoxic agent for hepatocellular carcinoma
Authors
KeywordsApoptosis
Chemocytotoxic
Gold(III) compound
Growth arrest and dna damage (Gadd) inducible genes
Hepatocellular carcinoma
Issue Date2006
PublisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/home
Citation
International Journal Of Cancer, 2006, v. 118 n. 6, p. 1527-1538 How to Cite?
AbstractRecently, a series of gold(III) meso-tetraarylporphyrins that are stable against demetallation in physiological conditions have been synthesized. In the present study, the antitumor effects of one of these compounds, gold(III) meso-tetraarylporphyrin 1a (gold-1a) was investigated in an orthotopic rat hepatocellular carcinoma (HCC) model as well as using a HCC cell line. The rat HCC model was induced by injection of rat hepatoma cells, McA-RH7777, into the left lobe of the liver. Seven days after tumor cell inoculation, gold-1a was injected directly into the tumor nodule at different doses, followed by the same doses via intraperitoneal injection twice a week. Gold-1a administration significantly prolonged the survival of HCC-bearing rats. Importantly, gold-la induced necrosis as well as apoptosis in the tumor tissues, but not in the normal liver tissues. Furthermore, gold-1a treatment neither caused significant drop in body weight of the rats nor affected plasma aspartate aminotransferase level. In the in vitro studies, we observed that gold-la treatment inhibited the proliferation of McA-RH7777 cells. Gold-1a upregulated genes that increase apoptosis, stabilize p53, decrease proliferation and downregulated genes playing roles in angiogenesis, invasion, and metabolism, as demonstrated by microarray. In particular, the compound upregulated 2 members of the growth arrest and DNA damage (Gadd) inducible gene family, Gadd34 and Gadd153. Suppression of Gadd34 and Gadd153 in McA-RH7777 cells by small hairpin RNA reduced the gold-1a-induced apoptosis and growth inhibition, indicating that gold-1a mediated its effects via upregulation of Gadd34 and Gadd153. Results from our study demonstrated that gold-1a might be a novel promising chemocytotoxic agent for treating HCC. © 2005 Wiley-Liss. Inc.
Persistent Identifierhttp://hdl.handle.net/10722/69033
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLum, CTen_HK
dc.contributor.authorYang, ZFen_HK
dc.contributor.authorLi, HYen_HK
dc.contributor.authorSun, RWYen_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorLin, MCMen_HK
dc.contributor.authorChe, CMen_HK
dc.contributor.authorKung, HFen_HK
dc.date.accessioned2010-09-06T06:09:56Z-
dc.date.available2010-09-06T06:09:56Z-
dc.date.issued2006en_HK
dc.identifier.citationInternational Journal Of Cancer, 2006, v. 118 n. 6, p. 1527-1538en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/69033-
dc.description.abstractRecently, a series of gold(III) meso-tetraarylporphyrins that are stable against demetallation in physiological conditions have been synthesized. In the present study, the antitumor effects of one of these compounds, gold(III) meso-tetraarylporphyrin 1a (gold-1a) was investigated in an orthotopic rat hepatocellular carcinoma (HCC) model as well as using a HCC cell line. The rat HCC model was induced by injection of rat hepatoma cells, McA-RH7777, into the left lobe of the liver. Seven days after tumor cell inoculation, gold-1a was injected directly into the tumor nodule at different doses, followed by the same doses via intraperitoneal injection twice a week. Gold-1a administration significantly prolonged the survival of HCC-bearing rats. Importantly, gold-la induced necrosis as well as apoptosis in the tumor tissues, but not in the normal liver tissues. Furthermore, gold-1a treatment neither caused significant drop in body weight of the rats nor affected plasma aspartate aminotransferase level. In the in vitro studies, we observed that gold-la treatment inhibited the proliferation of McA-RH7777 cells. Gold-1a upregulated genes that increase apoptosis, stabilize p53, decrease proliferation and downregulated genes playing roles in angiogenesis, invasion, and metabolism, as demonstrated by microarray. In particular, the compound upregulated 2 members of the growth arrest and DNA damage (Gadd) inducible gene family, Gadd34 and Gadd153. Suppression of Gadd34 and Gadd153 in McA-RH7777 cells by small hairpin RNA reduced the gold-1a-induced apoptosis and growth inhibition, indicating that gold-1a mediated its effects via upregulation of Gadd34 and Gadd153. Results from our study demonstrated that gold-1a might be a novel promising chemocytotoxic agent for treating HCC. © 2005 Wiley-Liss. Inc.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc.. The Journal's web site is located at http://www3.interscience.wiley.com/journal/29331/homeen_HK
dc.relation.ispartofInternational Journal of Canceren_HK
dc.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc.en_HK
dc.subjectApoptosisen_HK
dc.subjectChemocytotoxicen_HK
dc.subjectGold(III) compounden_HK
dc.subjectGrowth arrest and dna damage (Gadd) inducible genesen_HK
dc.subjectHepatocellular carcinomaen_HK
dc.titleGold(III) compound is a novel chemocytotoxic agent for hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0020-7136&volume=118&issue=6&spage=1527&epage=1538&date=2006&atitle=Gold(III)+compound+is+a+novel+chemocytotoxic+agent+for+hepatocellular+carcinomaen_HK
dc.identifier.emailLum, CT: ctlum@graduate.hku.hken_HK
dc.identifier.emailSun, RWY: rwysun@hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.emailPoon, RTP: poontp@hkucc.hku.hken_HK
dc.identifier.emailLin, MCM: mcllin@hkucc.hku.hken_HK
dc.identifier.emailChe, CM: cmche@hku.hken_HK
dc.identifier.authorityLum, CT=rp00757en_HK
dc.identifier.authoritySun, RWY=rp00781en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityLin, MCM=rp00746en_HK
dc.identifier.authorityChe, CM=rp00670en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/ijc.21484en_HK
dc.identifier.pmid16206274-
dc.identifier.scopuseid_2-s2.0-33644532836en_HK
dc.identifier.hkuros114281en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33644532836&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume118en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1527en_HK
dc.identifier.epage1538en_HK
dc.identifier.isiWOS:000235477100027-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLum, CT=7006889374en_HK
dc.identifier.scopusauthoridYang, ZF=39863860200en_HK
dc.identifier.scopusauthoridLi, HY=49763405100en_HK
dc.identifier.scopusauthoridSun, RWY=26325835800en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.scopusauthoridPoon, RTP=7103097223en_HK
dc.identifier.scopusauthoridLin, MCM=7404816359en_HK
dc.identifier.scopusauthoridChe, CM=7102442791en_HK
dc.identifier.scopusauthoridKung, HF=7402514190en_HK

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