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Article: Interferon-γ regulation of TNFα-induced matrix metalloproteinase 3 expression and migration of human glioma T98G cells

TitleInterferon-γ regulation of TNFα-induced matrix metalloproteinase 3 expression and migration of human glioma T98G cells
Authors
KeywordsGlioma
IFNγ
Invasiveness
MMP-3
TNFα
Issue Date2007
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, 2007, v. 121 n. 6, p. 1190-1196 How to Cite?
AbstractInduction of proinflammatory cytokines in response to malignant cells is an integral component of immune response to control tumor development. However, recent evidences have suggested that tumor cells may evade the immune system and exploit inflammatory responses to enhance its own growth. An exemplary example is the highly invasive and tumor necrosis factor (TNF)α-resistant glioblastoma, whose growth is associated with TNFα expression. We thus examined whether the tumor takes advantage of TNFα overexpression to enhance its invasiveness. To delineate the contribution of inflammation in tumor migration, we demonstrated that the role of proinflammatory cytokines on matrix metalloproteinases-3 (MMP-3) expression, and its consequent effects on the invasiveness of a human glioma cell-line, T98G. By using Matrigel Invasion Chamber, T98G cell migration was significantly enhanced in response to TNFα. In contrast, interferon-γ (IFNγ) reduced both basal and TNFα-enhanced cell invasion. To investigate the mechanisms involved, we demonstrated that TNFα upregulated mRNA and protein expression of MMP-3 in T98G cells, whereas IFNγ downregulated the MMP-3 expression. The role of MMP-3 in glioma invasiveness was further confirmed by transfecting MMP-3 siRNA in T98G to abrogate the TNFα-enhanced cell invasion. To delineate the mechanisms further, we showed that IFNγ exerts an inhibitory effect on the binding of TNFα-activated Ets-1 and NFκB to their respective enhancer elements found in MMP-3 promoter. In summary, our results indicated that TNFα enhances the invasiveness of T98G glioma cells through MMP-3 induction, and such enhancement of cell migration can be inhibited by IFNγ. © 2007 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/79914
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorCheng, SMen_HK
dc.contributor.authorXing, Ben_HK
dc.contributor.authorLi, JCBen_HK
dc.contributor.authorCheung, BKWen_HK
dc.contributor.authorLau, ASYen_HK
dc.date.accessioned2010-09-06T08:00:14Z-
dc.date.available2010-09-06T08:00:14Z-
dc.date.issued2007en_HK
dc.identifier.citationInternational Journal Of Cancer, 2007, v. 121 n. 6, p. 1190-1196en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/79914-
dc.description.abstractInduction of proinflammatory cytokines in response to malignant cells is an integral component of immune response to control tumor development. However, recent evidences have suggested that tumor cells may evade the immune system and exploit inflammatory responses to enhance its own growth. An exemplary example is the highly invasive and tumor necrosis factor (TNF)α-resistant glioblastoma, whose growth is associated with TNFα expression. We thus examined whether the tumor takes advantage of TNFα overexpression to enhance its invasiveness. To delineate the contribution of inflammation in tumor migration, we demonstrated that the role of proinflammatory cytokines on matrix metalloproteinases-3 (MMP-3) expression, and its consequent effects on the invasiveness of a human glioma cell-line, T98G. By using Matrigel Invasion Chamber, T98G cell migration was significantly enhanced in response to TNFα. In contrast, interferon-γ (IFNγ) reduced both basal and TNFα-enhanced cell invasion. To investigate the mechanisms involved, we demonstrated that TNFα upregulated mRNA and protein expression of MMP-3 in T98G cells, whereas IFNγ downregulated the MMP-3 expression. The role of MMP-3 in glioma invasiveness was further confirmed by transfecting MMP-3 siRNA in T98G to abrogate the TNFα-enhanced cell invasion. To delineate the mechanisms further, we showed that IFNγ exerts an inhibitory effect on the binding of TNFα-activated Ets-1 and NFκB to their respective enhancer elements found in MMP-3 promoter. In summary, our results indicated that TNFα enhances the invasiveness of T98G glioma cells through MMP-3 induction, and such enhancement of cell migration can be inhibited by IFNγ. © 2007 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.rightsInternational Journal of Cancer. Copyright © John Wiley & Sons, Inc.-
dc.subjectGliomaen_HK
dc.subjectIFNγen_HK
dc.subjectInvasivenessen_HK
dc.subjectMMP-3en_HK
dc.subjectTNFαen_HK
dc.titleInterferon-γ regulation of TNFα-induced matrix metalloproteinase 3 expression and migration of human glioma T98G cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0020-7136&volume=121&spage=1190&epage=6&date=2007&atitle=Interferon-gamma+regulation+of+TNF-alpha-induced+matrix+metalloproteinase+3+expression+and+migration+of+human+glioma+T98G+cells.en_HK
dc.identifier.emailLi, JCB: jamesli@hku.hken_HK
dc.identifier.emailLau, ASY: asylau@hku.hken_HK
dc.identifier.authorityLi, JCB=rp00496en_HK
dc.identifier.authorityLau, ASY=rp00474en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.22729en_HK
dc.identifier.pmid17520672en_HK
dc.identifier.scopuseid_2-s2.0-34548076607en_HK
dc.identifier.hkuros138663en_HK
dc.identifier.hkuros132364-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34548076607&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume121en_HK
dc.identifier.issue6en_HK
dc.identifier.spage1190en_HK
dc.identifier.epage1196en_HK
dc.identifier.isiWOS:000248976800004-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridCheng, SM=19638747100en_HK
dc.identifier.scopusauthoridXing, B=7005212013en_HK
dc.identifier.scopusauthoridLi, JCB=23103447500en_HK
dc.identifier.scopusauthoridCheung, BKW=9634391200en_HK
dc.identifier.scopusauthoridLau, ASY=7202626202en_HK

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