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Article: Mechanism of metastasis by membrane type 1-matrix metalloproteinase in hepatocellular carcinoma

TitleMechanism of metastasis by membrane type 1-matrix metalloproteinase in hepatocellular carcinoma
Authors
KeywordsInvasion
Liver cancer
Metastasis
MT1-MMP/MMP14
Issue Date2005
PublisherBaishideng Publishing Group. The Journal's web site is located at http://www.wjgnet.com/1007-9327/index.htm
Citation
World Journal Of Gastroenterology, 2005, v. 11 n. 40, p. 6269-6276 How to Cite?
AbstractAim: To investigate the precise role of membrane type 1-matrix metalloproteinase (MT1-MMP) in hepatocellular carcinoma (HCC) metastasis. Methods: Human HCC cells Hep3B with overexpression of MT1-MMP were established by stable transfection, and compared with control cells carrying the empty vector. Cells were examined in vivo for their differences in the metastatic ability of athymic nude mice, and analyzed in vitro for their differences in invasion ability by invasion chamber coated with Matrigel,adhesion towards collagen I and migration through culture chamber. Cell proliferation and apoptosis in adherent and suspension status were evaluated by MTT and flow cytometry analysis. Results: We found that overexpression of MT1-MMP could increase intrahepatic metastasis in nude mice with orthotopic implantation of HCC cells (incidence of 100% [MT1-MMP transfectants] vs 40% [vector control transfectants], P<0.05). MT1-MMP could also enhance cell invasion through Matrigel (107.7 vs39.3 cells/field, P<0.001), adhesion towards matrix (0.30 vs 0.12 absorbance unit at 540 nm, P<0.001), cell migration (89.3 vs 39.0 cells/field, P<0.001), and cell proliferation (24.3 vs 40.5 h/doubling, P<0.001). We also observed that MT1-MMP supported cell survival (71.4% vs 23.9%, P<0.001) with reduced apoptosis (43.7% vs 51.0%, P<0.05) in an attachment-free environment. Conclusion: MT1-MMP overexpression could enhance metastasis. In addition to its active role in matrix degradation during tumor invasion, MT1-MMP enhances tumor cell survival upon challenge of detachment, which is important during metastasis when cells enter the circulation. © 2005 The WJG Press and Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/83302
ISSN
2015 Impact Factor: 2.787
2015 SCImago Journal Rankings: 1.076
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorIp, YCen_HK
dc.contributor.authorCheung, STen_HK
dc.contributor.authorLeung, KLen_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T08:39:24Z-
dc.date.available2010-09-06T08:39:24Z-
dc.date.issued2005en_HK
dc.identifier.citationWorld Journal Of Gastroenterology, 2005, v. 11 n. 40, p. 6269-6276en_HK
dc.identifier.issn1007-9327en_HK
dc.identifier.urihttp://hdl.handle.net/10722/83302-
dc.description.abstractAim: To investigate the precise role of membrane type 1-matrix metalloproteinase (MT1-MMP) in hepatocellular carcinoma (HCC) metastasis. Methods: Human HCC cells Hep3B with overexpression of MT1-MMP were established by stable transfection, and compared with control cells carrying the empty vector. Cells were examined in vivo for their differences in the metastatic ability of athymic nude mice, and analyzed in vitro for their differences in invasion ability by invasion chamber coated with Matrigel,adhesion towards collagen I and migration through culture chamber. Cell proliferation and apoptosis in adherent and suspension status were evaluated by MTT and flow cytometry analysis. Results: We found that overexpression of MT1-MMP could increase intrahepatic metastasis in nude mice with orthotopic implantation of HCC cells (incidence of 100% [MT1-MMP transfectants] vs 40% [vector control transfectants], P<0.05). MT1-MMP could also enhance cell invasion through Matrigel (107.7 vs39.3 cells/field, P<0.001), adhesion towards matrix (0.30 vs 0.12 absorbance unit at 540 nm, P<0.001), cell migration (89.3 vs 39.0 cells/field, P<0.001), and cell proliferation (24.3 vs 40.5 h/doubling, P<0.001). We also observed that MT1-MMP supported cell survival (71.4% vs 23.9%, P<0.001) with reduced apoptosis (43.7% vs 51.0%, P<0.05) in an attachment-free environment. Conclusion: MT1-MMP overexpression could enhance metastasis. In addition to its active role in matrix degradation during tumor invasion, MT1-MMP enhances tumor cell survival upon challenge of detachment, which is important during metastasis when cells enter the circulation. © 2005 The WJG Press and Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherBaishideng Publishing Group. The Journal's web site is located at http://www.wjgnet.com/1007-9327/index.htmen_HK
dc.relation.ispartofWorld Journal of Gastroenterologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subjectInvasionen_HK
dc.subjectLiver canceren_HK
dc.subjectMetastasisen_HK
dc.subjectMT1-MMP/MMP14en_HK
dc.titleMechanism of metastasis by membrane type 1-matrix metalloproteinase in hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1007-9327&volume=11&issue=40&spage=6269&epage=6276&date=2005&atitle=Mechanism+of+metastasis+by+membrane+type+1-matrix+metalloproteinase+in+hepatocellular+carcinomaen_HK
dc.identifier.emailCheung, ST: stcheung@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityCheung, ST=rp00457en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3748/wjg.v11.i40.6269-
dc.identifier.pmid16419154-
dc.identifier.pmcidPMC4320329-
dc.identifier.scopuseid_2-s2.0-29544433753en_HK
dc.identifier.hkuros116944en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-29544433753&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume11en_HK
dc.identifier.issue40en_HK
dc.identifier.spage6269en_HK
dc.identifier.epage6276en_HK
dc.identifier.isiWOS:000208318000006-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridIp, YC=36943517300en_HK
dc.identifier.scopusauthoridCheung, ST=7202473497en_HK
dc.identifier.scopusauthoridLeung, KL=10438768800en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK

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