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Article: FTY720 suppresses liver tumor metastasis by reducing the population of circulating endothelial progenitor cells

TitleFTY720 suppresses liver tumor metastasis by reducing the population of circulating endothelial progenitor cells
Authors
KeywordsAnimal cell
Antineoplastic activity
Blood sampling
Cell count
Circulating tumor cell
Issue Date2012
PublisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.action
Citation
Plos One, 2012, v. 7 n. 2 How to Cite?
AbstractBackground: Surgical procedures such as liver resection and liver transplantation are the first-line treatments for hepatocellular carcinoma (HCC) patients. However, the high incidence of tumor recurrence and metastasis after liver surgery remains a major problem. Recent studies have shown that hepatic ischemia-reperfusion (I/R) injury and endothelial progenitor cells (EPCs) contribute to tumor growth and metastasis. We aim to investigate the mechanism of FTY720, which was originally applied as an immunomodulator, on suppression of liver tumor metastasis after liver resection and partial hepatic I/R injury. Methodology/Principal Findings: An orthotopic liver tumor model in Buffalo rat was established using the hepatocellular carcinoma cell line McA-RH7777. Two weeks after orthotopic liver tumor implantation, the rats underwent liver resection for tumor-bearing lobe and partial hepatic I/R injury. FTY720 (2 mg/kg) was administered through the inferior caval vein before and after I/R injury. Blood samples were taken at days 0, 1, 3, 7, 14, 21 and 28 for detection of circulating EPCs (CD133+CD34+). Our results showed that intrahepatic and lung metastases were significantly inhibited together with less tumor angiogenesis by FTY720 treatment. The number of circulating EPCs was also significantly decreased by FTY720 treatment from day 7 to day 28. Hepatic gene expressions of CXCL10, VEGF, CXCR3, CXCR4 induced by hepatic I/R injury were down-regulated in the treatment group. Conclusions/Significance: FTY720 suppressed liver tumor metastasis after liver resection marred by hepatic I/R injury in a rat liver tumor model by attenuating hepatic I/R injury and reducing circulating EPCs. © 2012 Li et al.
Persistent Identifierhttp://hdl.handle.net/10722/152872
ISSN
2015 Impact Factor: 3.057
2015 SCImago Journal Rankings: 1.395
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant Council Hong KongHKU5/CRF/08
HKU1/CRF10
HKU3/CRF11R
Centre for Cancer Research-Strategy Research Theme of the University of Hong Kong
Funding Information:

This study was supported by the Collaborative Research Funds (HKU5/CRF/08, HKU1/CRF10 & HKU3/CRF11R) of the Research Grant Council Hong Kong, Small project funding and Seed funding of Centre for Cancer Research-Strategy Research Theme programme of the University of Hong Kong. The funder had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

References
Grants

 

DC FieldValueLanguage
dc.contributor.authorLi, CXen_HK
dc.contributor.authorShao, Yen_HK
dc.contributor.authorNg, KTPen_HK
dc.contributor.authorLiu, XBen_HK
dc.contributor.authorLing, CCen_HK
dc.contributor.authorMa, YYen_HK
dc.contributor.authorGeng, Wen_HK
dc.contributor.authorFan, STen_HK
dc.contributor.authorLo, CMen_HK
dc.contributor.authorMan, Ken_HK
dc.date.accessioned2012-07-16T09:51:04Z-
dc.date.available2012-07-16T09:51:04Z-
dc.date.issued2012en_HK
dc.identifier.citationPlos One, 2012, v. 7 n. 2en_HK
dc.identifier.issn1932-6203en_HK
dc.identifier.urihttp://hdl.handle.net/10722/152872-
dc.description.abstractBackground: Surgical procedures such as liver resection and liver transplantation are the first-line treatments for hepatocellular carcinoma (HCC) patients. However, the high incidence of tumor recurrence and metastasis after liver surgery remains a major problem. Recent studies have shown that hepatic ischemia-reperfusion (I/R) injury and endothelial progenitor cells (EPCs) contribute to tumor growth and metastasis. We aim to investigate the mechanism of FTY720, which was originally applied as an immunomodulator, on suppression of liver tumor metastasis after liver resection and partial hepatic I/R injury. Methodology/Principal Findings: An orthotopic liver tumor model in Buffalo rat was established using the hepatocellular carcinoma cell line McA-RH7777. Two weeks after orthotopic liver tumor implantation, the rats underwent liver resection for tumor-bearing lobe and partial hepatic I/R injury. FTY720 (2 mg/kg) was administered through the inferior caval vein before and after I/R injury. Blood samples were taken at days 0, 1, 3, 7, 14, 21 and 28 for detection of circulating EPCs (CD133+CD34+). Our results showed that intrahepatic and lung metastases were significantly inhibited together with less tumor angiogenesis by FTY720 treatment. The number of circulating EPCs was also significantly decreased by FTY720 treatment from day 7 to day 28. Hepatic gene expressions of CXCL10, VEGF, CXCR3, CXCR4 induced by hepatic I/R injury were down-regulated in the treatment group. Conclusions/Significance: FTY720 suppressed liver tumor metastasis after liver resection marred by hepatic I/R injury in a rat liver tumor model by attenuating hepatic I/R injury and reducing circulating EPCs. © 2012 Li et al.en_HK
dc.languageengen_US
dc.publisherPublic Library of Science. The Journal's web site is located at http://www.plosone.org/home.actionen_HK
dc.relation.ispartofPLoS ONEen_HK
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectAnimal cell-
dc.subjectAntineoplastic activity-
dc.subjectBlood sampling-
dc.subjectCell count-
dc.subjectCirculating tumor cell-
dc.titleFTY720 suppresses liver tumor metastasis by reducing the population of circulating endothelial progenitor cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailNg, KTP: ledodes@hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.emailMan, K: kwanman@hku.hken_HK
dc.identifier.authorityNg, KTP=rp01720en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1371/journal.pone.0032380en_HK
dc.identifier.pmid22384233-
dc.identifier.pmcidPMC3288101-
dc.identifier.scopuseid_2-s2.0-84863291987en_HK
dc.identifier.hkuros206126en_US
dc.identifier.hkuros200783en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84863291987&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume7en_HK
dc.identifier.issue2en_HK
dc.identifier.isiWOS:000302918500082-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectLiver Transplantation Research Centre: A Multidisciplinary Study for Liver Graft Injury-
dc.identifier.scopusauthoridLi, CX=55277237900en_HK
dc.identifier.scopusauthoridShao, Y=55277521000en_HK
dc.identifier.scopusauthoridNg, KTP=7403178513en_HK
dc.identifier.scopusauthoridLiu, XB=17435186900en_HK
dc.identifier.scopusauthoridLing, CC=55277226600en_HK
dc.identifier.scopusauthoridMa, YY=55276973000en_HK
dc.identifier.scopusauthoridGeng, W=54412151800en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK
dc.identifier.scopusauthoridLo, CM=55261732500en_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.citeulike10413826-

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