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Conference Paper: Inflammatory microenvironment accelerates liver tumor growth and metastasis by mobilizing circulating endothelial progenitor cells and increasing cancer stem like cell populations

TitleInflammatory microenvironment accelerates liver tumor growth and metastasis by mobilizing circulating endothelial progenitor cells and increasing cancer stem like cell populations
Authors
KeywordsMedical sciences
Gastroenterology medical sciences
Surgery
Issue Date2009
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jtoc/106570021
Citation
The 15th Annual International Congres of the International Liver Transplantation Society (ILTS 2009), New York, NY., 8-11 July 2009. In Liver Transplantation, 2009, v. 15, suppl. s7, p. S97, abstract no. O-84 How to Cite?
AbstractOBJECTIVE: We aim to explore the mechanism of liver tumor growth and metastasis under inflammatory microenvironment by studying the direct role of hepatic I/R injury on mobilization of circulating endothelial progenitor cells (EPCs) and promotion of stemness features of liver cancer cell itself. METHODS: Small numbers of rat liver tumor cells (CRL1601, 500-1000 cells) were injected into right portal vein of male Buffalo rats with or without partial hepatic I/R injury (20/20 minutes duration on right and median lobes). The tumor growth and metastases were longitudinally monitored by Xenogen in vivo imaging system (IVIS) in live animals by detection of luminance signals from tumor cells. Blood samples were taken at day1, 7, 14, 21 and 28 for detection of EPCs (CD133+CD34+) and cancer stem like cells-CSCs (CD133+CD90+, CD133+EpCAM+, CD90+EpCAM+). The proportions of CSCs were also compared in rat liver tumor tissues. To confirm the invasive features of the tumor developed in inflammatory microenvironment induced by hepatic I/R injury, the rat liver tumors were further orthotopically implanted into the liver of nude mice. The nude mice tumor growth/metastasis and circulating EPCs/CSCs were compared. RESULTS: Aggressive and early rat liver tumor development and metastasis were mainly found in I/R injury group. Significant higher levels of IP10/ MIP2/VEGF induced by hepatic I/R injury subsequently mobilized EPCs (CD133+CD34+) to circulation compared to the control group (day1: 35 vs 12/10^5cells, p=0.004; day7: 64 vs 38/10^5cells, p=0.025; day21: 24 vs 9/10^5cells, p=0.028; day28: 18 vs 12/10^5cells, p=0.006). CD133+ cells were also found in lung metastatic nodules in I/R injury group. The numbers of circulation and tumor CSCs were also significantly increased in I/R injury group (Circulation: day 1:23.5 vs7/10^5cells, p=0.006; day28: 18.5 vs 5/10^5cells, p=0.006; Rat tumor: 290 vs 40/10^5cells, p=0.047). The nude mice implanted with tumor from I/R injury group also had higher circulation levels of EPCs (17 vs 4/10^5cells, p=0.004) and CSCs (43 vs 0/10^5cells, p=0.01). Their aggressive tumor growth and metastasis were also confirmed. CONCLUSION: Inflammatory microenvironment promoted liver tumor growth and metastasis by increasing cancer stem like cell populations and mobilizating circulating endothelial progenitor cells.
Persistent Identifierhttp://hdl.handle.net/10722/107808
ISSN
2015 Impact Factor: 3.951
2015 SCImago Journal Rankings: 1.763

 

DC FieldValueLanguage
dc.contributor.authorMan, Ken_HK
dc.contributor.authorCheng, Qen_HK
dc.contributor.authorLiu, Yen_HK
dc.contributor.authorLam, TTen_HK
dc.contributor.authorNg, KTPen_HK
dc.contributor.authorLo, CMen_HK
dc.date.accessioned2010-09-26T00:13:15Z-
dc.date.available2010-09-26T00:13:15Z-
dc.date.issued2009en_HK
dc.identifier.citationThe 15th Annual International Congres of the International Liver Transplantation Society (ILTS 2009), New York, NY., 8-11 July 2009. In Liver Transplantation, 2009, v. 15, suppl. s7, p. S97, abstract no. O-84en_HK
dc.identifier.issn1527-6465-
dc.identifier.urihttp://hdl.handle.net/10722/107808-
dc.description.abstractOBJECTIVE: We aim to explore the mechanism of liver tumor growth and metastasis under inflammatory microenvironment by studying the direct role of hepatic I/R injury on mobilization of circulating endothelial progenitor cells (EPCs) and promotion of stemness features of liver cancer cell itself. METHODS: Small numbers of rat liver tumor cells (CRL1601, 500-1000 cells) were injected into right portal vein of male Buffalo rats with or without partial hepatic I/R injury (20/20 minutes duration on right and median lobes). The tumor growth and metastases were longitudinally monitored by Xenogen in vivo imaging system (IVIS) in live animals by detection of luminance signals from tumor cells. Blood samples were taken at day1, 7, 14, 21 and 28 for detection of EPCs (CD133+CD34+) and cancer stem like cells-CSCs (CD133+CD90+, CD133+EpCAM+, CD90+EpCAM+). The proportions of CSCs were also compared in rat liver tumor tissues. To confirm the invasive features of the tumor developed in inflammatory microenvironment induced by hepatic I/R injury, the rat liver tumors were further orthotopically implanted into the liver of nude mice. The nude mice tumor growth/metastasis and circulating EPCs/CSCs were compared. RESULTS: Aggressive and early rat liver tumor development and metastasis were mainly found in I/R injury group. Significant higher levels of IP10/ MIP2/VEGF induced by hepatic I/R injury subsequently mobilized EPCs (CD133+CD34+) to circulation compared to the control group (day1: 35 vs 12/10^5cells, p=0.004; day7: 64 vs 38/10^5cells, p=0.025; day21: 24 vs 9/10^5cells, p=0.028; day28: 18 vs 12/10^5cells, p=0.006). CD133+ cells were also found in lung metastatic nodules in I/R injury group. The numbers of circulation and tumor CSCs were also significantly increased in I/R injury group (Circulation: day 1:23.5 vs7/10^5cells, p=0.006; day28: 18.5 vs 5/10^5cells, p=0.006; Rat tumor: 290 vs 40/10^5cells, p=0.047). The nude mice implanted with tumor from I/R injury group also had higher circulation levels of EPCs (17 vs 4/10^5cells, p=0.004) and CSCs (43 vs 0/10^5cells, p=0.01). Their aggressive tumor growth and metastasis were also confirmed. CONCLUSION: Inflammatory microenvironment promoted liver tumor growth and metastasis by increasing cancer stem like cell populations and mobilizating circulating endothelial progenitor cells.-
dc.languageengen_HK
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www3.interscience.wiley.com/cgi-bin/jtoc/106570021-
dc.relation.ispartofLiver Transplantationen_HK
dc.rightsLiver Transplantation. Copyright © John Wiley & Sons, Inc.-
dc.subjectMedical sciences-
dc.subjectGastroenterology medical sciences-
dc.subjectSurgery-
dc.titleInflammatory microenvironment accelerates liver tumor growth and metastasis by mobilizing circulating endothelial progenitor cells and increasing cancer stem like cell populationsen_HK
dc.typeConference_Paperen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1527-6465&volume=15&issue=suppl. 7&spage=s97&epage=&date=2009&atitle=Inflammatory+microenvironment+accelerates+liver+tumor+growth+and+metastasis+by+mobilizing+circulating+endothelial+progenitor+cells+and+increasing+cancer+stem+like+cell+populations-
dc.identifier.emailMan, K: kwanman@hkucc.hku.hken_HK
dc.identifier.emailCheng, Q: qiaocheng@hotmail.comen_HK
dc.identifier.emailLam, TT: ttlams@hotmail.comen_HK
dc.identifier.emailNg, KTP: ledodes@hkucc.hku.hken_HK
dc.identifier.emailLo, CM: chungmlo@hkucc.hku.hken_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityLo, CM=rp00412en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1002/lt.21830-
dc.identifier.hkuros161635en_HK
dc.identifier.hkuros170114-
dc.identifier.volume15en_HK
dc.identifier.issuesuppl. s7en_HK
dc.identifier.spageS97, abstract no. O-84en_HK
dc.identifier.epageS97, abstract no. O-84-
dc.description.otherThe 15th Annual International Congres of the International Liver Transplantation Society (ILTS), New York, N.Y., 8-11 July 2009. In Liver Transplantation, 2009, v. 15, suppl. 7, p. s97, abstract no. O-84-

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