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Article: Ischemia-reperfusion of small liver remnant promotes liver tumor growth and metastases - Activation of cell invasion and migration pathways

TitleIschemia-reperfusion of small liver remnant promotes liver tumor growth and metastases - Activation of cell invasion and migration pathways
Authors
Issue Date2007
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jtoc/106570021
Citation
Liver Transplantation, 2007, v. 13 n. 12, p. 1669-1677 How to Cite?
AbstractElucidating the mechanism of liver tumor growth and metastasis after hepatic ischemia-reperfusion (I/R) injury of a small liver remnant will lay the foundation for the development of therapeutic strategies to target small liver remnant injury, and will reduce the likelihood of tumor recurrence after major hepatectomy or liver transplantation for liver cancer patients. In the current study, we aimed to investigate the effect of hepatic I/R injury of a small liver remnant on liver tumor development and metastases, and to explore the precise molecular mechanisms. A rat liver tumor model that underwent partial hepatic I/R injury with or without major hepatectomy was investigated. Liver tumor growth and metastases were compared among the groups with different surgical stress. An orthotopic liver tumor nude mice model was used to further confirm the invasiveness of the tumor cells from the above rat liver tumor model. Significant tumor growth and intrahepatic metastasis (5 of 6 vs. 0 of 6, P = 0.015), and lung metastasis (5 of 6 vs. 0 of 6, P = 0.015) were found in rats undergoing I/R and major hepatectomy compared with the control group, and was accompanied by upregulation of mRNA levels for Cdc42, ROCK (Rho kinase), and vascular endothelial growth factor, as well as activation of hepatic stellate cells. Most of the nude mice implanted with liver tumor from rats under I/R injury and major hepatectomy developed intrahepatic and lung metastases. In conclusion, hepatic I/R injury of a small liver remnant exacerbated liver tumor growth and metastasis by marked activation of cell adhesion, invasion, and angiogenesis pathways. © 2007 AASLD.
DescriptionComment in Liver Transpl. 2007 Dec;13(12):1623-1626
Persistent Identifierhttp://hdl.handle.net/10722/84533
ISSN
2015 Impact Factor: 3.951
2015 SCImago Journal Rankings: 1.763
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorMan, Ken_HK
dc.contributor.authorNg, KTen_HK
dc.contributor.authorLo, CMen_HK
dc.contributor.authorHo, JWen_HK
dc.contributor.authorSun, BSen_HK
dc.contributor.authorSun, CKen_HK
dc.contributor.authorLee, TKen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T08:54:04Z-
dc.date.available2010-09-06T08:54:04Z-
dc.date.issued2007en_HK
dc.identifier.citationLiver Transplantation, 2007, v. 13 n. 12, p. 1669-1677en_HK
dc.identifier.issn1527-6465en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84533-
dc.descriptionComment in Liver Transpl. 2007 Dec;13(12):1623-1626-
dc.description.abstractElucidating the mechanism of liver tumor growth and metastasis after hepatic ischemia-reperfusion (I/R) injury of a small liver remnant will lay the foundation for the development of therapeutic strategies to target small liver remnant injury, and will reduce the likelihood of tumor recurrence after major hepatectomy or liver transplantation for liver cancer patients. In the current study, we aimed to investigate the effect of hepatic I/R injury of a small liver remnant on liver tumor development and metastases, and to explore the precise molecular mechanisms. A rat liver tumor model that underwent partial hepatic I/R injury with or without major hepatectomy was investigated. Liver tumor growth and metastases were compared among the groups with different surgical stress. An orthotopic liver tumor nude mice model was used to further confirm the invasiveness of the tumor cells from the above rat liver tumor model. Significant tumor growth and intrahepatic metastasis (5 of 6 vs. 0 of 6, P = 0.015), and lung metastasis (5 of 6 vs. 0 of 6, P = 0.015) were found in rats undergoing I/R and major hepatectomy compared with the control group, and was accompanied by upregulation of mRNA levels for Cdc42, ROCK (Rho kinase), and vascular endothelial growth factor, as well as activation of hepatic stellate cells. Most of the nude mice implanted with liver tumor from rats under I/R injury and major hepatectomy developed intrahepatic and lung metastases. In conclusion, hepatic I/R injury of a small liver remnant exacerbated liver tumor growth and metastasis by marked activation of cell adhesion, invasion, and angiogenesis pathways. © 2007 AASLD.en_HK
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jtoc/106570021en_HK
dc.relation.ispartofLiver Transplantationen_HK
dc.rightsLiver Transplantation. Copyright © John Wiley & Sons, Inc.en_HK
dc.subject.meshHepatectomy - adverse effects-
dc.subject.meshLiver - blood supply - metabolism - pathology - surgery-
dc.subject.meshLiver Neoplasms, Experimental - metabolism - pathology - surgery-
dc.subject.meshLung Neoplasms - etiology - metabolism - secondary-
dc.subject.meshNeoplasm Recurrence, Local - etiology - metabolism - pathology-
dc.titleIschemia-reperfusion of small liver remnant promotes liver tumor growth and metastases - Activation of cell invasion and migration pathwaysen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1527-6465&volume=13&issue=12&spage=1669&epage=1677&date=2007&atitle=Ischemia-reperfusion+of+small+liver+remnant+promotes+liver+tumor+growth+and+metastases+-+activation+of+cell+invasion+and+migration+pathwaysen_HK
dc.identifier.emailMan, K: kwanman@hku.hken_HK
dc.identifier.emailNg, KT: ledodes@hku.hken_HK
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hken_HK
dc.identifier.emailLee, TK: tkwlee@hkucc.hku.hken_HK
dc.identifier.emailPoon, RTP: poontp@hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityNg, KT=rp01720en_HK
dc.identifier.authorityLo, CM=rp00412en_HK
dc.identifier.authorityLee, TK=rp00447en_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/lt.21193en_HK
dc.identifier.pmid18044786-
dc.identifier.scopuseid_2-s2.0-37549030135en_HK
dc.identifier.hkuros144255en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-37549030135&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume13en_HK
dc.identifier.issue12en_HK
dc.identifier.spage1669en_HK
dc.identifier.epage1677en_HK
dc.identifier.isiWOS:000251574100009-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.scopusauthoridNg, KT=7403178513en_HK
dc.identifier.scopusauthoridLo, CM=7401771672en_HK
dc.identifier.scopusauthoridHo, JW=7402649982en_HK
dc.identifier.scopusauthoridSun, BS=23101636500en_HK
dc.identifier.scopusauthoridSun, CK=7404248685en_HK
dc.identifier.scopusauthoridLee, TK=7501439435en_HK
dc.identifier.scopusauthoridPoon, RTP=7103097223en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK

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