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Article: Macrophage migration inhibitory factor: Roles in regulating tumor cell migration and expression of angiogenic factors in hepatocellular carcinoma

TitleMacrophage migration inhibitory factor: Roles in regulating tumor cell migration and expression of angiogenic factors in hepatocellular carcinoma
Authors
KeywordsAngiogenesis
Hepatocellular carcinoma
Macrophage migration inhibitory factor
Metastasis
Issue Date2003
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, 2003, v. 107 n. 1, p. 22-29 How to Cite?
AbstractMacrophage migration inhibitory factor (MIF) may contribute to multiple aspects of tumor progression, including control of cell proliferation, differentiation, cell survival and angiogenesis. However, the potential roles of MIF in regulating hepatocellular carcinoma (HCC) tumor cell migration and the expression of angiogenic factors by HCC tumor cells have not been studied yet. In our study, we reported that intracellular MIF mRNA and protein were overexpressed in HCC tissues compared to nontumor tissues by using in situ hybridization and immunohistochemic staining. HCC tumor cell lines also secreted large amounts of MIF into the supernatants of tumor cell culture. To assess the role of MIF in HCC, we employed the transwell invasion chamber to study the effect of MIF on tumor cell migration. Our results showed that recombinant MIF and the supernatants of tumor cell line culture could enhance the invasion and migration of HCC cells. This effect can be inhibited by the addition of a neutralizing anti-MIF antibody. We observed that increased MIF serum levels correlated with higher levels of interleukin-8 (IL-8) in the sera of patients with HCC than in normal volunteers. We therefore hypothesized that MIF may regulate the production of angiogenic factors by HCC cells. To test this hypothesis, we examined the effect of MIF treatment on vascular endothelial growth factor (VF) and IL-8 expression by HCC cell lines. MIF induced a significant dose-dependent increase in IL-8 and VEGF production. Taken together, our results indicated that MIF may act as an autocrine-acting factor that stimulates angiogenesis and metastasis in HCC by promoting expression of angiogenic factors and migration of tumor cells. A more detailed understanding of the MIF regulatory mechanisms involved may provide insight into new direction in the treatment of HCC. © 2003 Wiley-Liss, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/88684
ISSN
2015 Impact Factor: 5.531
2015 SCImago Journal Rankings: 2.657
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorRen, Yen_HK
dc.contributor.authorTsui, HTen_HK
dc.contributor.authorPoon, RTPen_HK
dc.contributor.authorNg, IOLen_HK
dc.contributor.authorLi, Zen_HK
dc.contributor.authorChen, Yen_HK
dc.contributor.authorJiang, Gen_HK
dc.contributor.authorLau, Cen_HK
dc.contributor.authorYu, WCen_HK
dc.contributor.authorBacher, Men_HK
dc.contributor.authorFan, STen_HK
dc.date.accessioned2010-09-06T09:46:37Z-
dc.date.available2010-09-06T09:46:37Z-
dc.date.issued2003en_HK
dc.identifier.citationInternational Journal Of Cancer, 2003, v. 107 n. 1, p. 22-29en_HK
dc.identifier.issn0020-7136en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88684-
dc.description.abstractMacrophage migration inhibitory factor (MIF) may contribute to multiple aspects of tumor progression, including control of cell proliferation, differentiation, cell survival and angiogenesis. However, the potential roles of MIF in regulating hepatocellular carcinoma (HCC) tumor cell migration and the expression of angiogenic factors by HCC tumor cells have not been studied yet. In our study, we reported that intracellular MIF mRNA and protein were overexpressed in HCC tissues compared to nontumor tissues by using in situ hybridization and immunohistochemic staining. HCC tumor cell lines also secreted large amounts of MIF into the supernatants of tumor cell culture. To assess the role of MIF in HCC, we employed the transwell invasion chamber to study the effect of MIF on tumor cell migration. Our results showed that recombinant MIF and the supernatants of tumor cell line culture could enhance the invasion and migration of HCC cells. This effect can be inhibited by the addition of a neutralizing anti-MIF antibody. We observed that increased MIF serum levels correlated with higher levels of interleukin-8 (IL-8) in the sera of patients with HCC than in normal volunteers. We therefore hypothesized that MIF may regulate the production of angiogenic factors by HCC cells. To test this hypothesis, we examined the effect of MIF treatment on vascular endothelial growth factor (VF) and IL-8 expression by HCC cell lines. MIF induced a significant dose-dependent increase in IL-8 and VEGF production. Taken together, our results indicated that MIF may act as an autocrine-acting factor that stimulates angiogenesis and metastasis in HCC by promoting expression of angiogenic factors and migration of tumor cells. A more detailed understanding of the MIF regulatory mechanisms involved may provide insight into new direction in the treatment of HCC. © 2003 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.subjectAngiogenesisen_HK
dc.subjectHepatocellular carcinomaen_HK
dc.subjectMacrophage migration inhibitory factoren_HK
dc.subjectMetastasisen_HK
dc.subject.meshAdulten_HK
dc.subject.meshAgeden_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshCarcinoma, Hepatocellular - metabolism - pathologyen_HK
dc.subject.meshCase-Control Studiesen_HK
dc.subject.meshCell Divisionen_HK
dc.subject.meshCell Movementen_HK
dc.subject.meshDose-Response Relationship, Drugen_HK
dc.subject.meshEndothelial Growth Factors - biosynthesis - geneticsen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshFlow Cytometryen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHumansen_HK
dc.subject.meshImmunoenzyme Techniquesen_HK
dc.subject.meshIn Situ Hybridizationen_HK
dc.subject.meshIntercellular Signaling Peptides and Proteins - biosynthesis - geneticsen_HK
dc.subject.meshInterleukin-8 - biosynthesis - geneticsen_HK
dc.subject.meshLiver Neoplasms - metabolism - pathologyen_HK
dc.subject.meshLymphokines - biosynthesis - geneticsen_HK
dc.subject.meshMacrophage Migration-Inhibitory Factors - pharmacology - physiologyen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiddle Ageden_HK
dc.subject.meshProspective Studiesen_HK
dc.subject.meshRNA, Messenger - metabolismen_HK
dc.subject.meshRNA, Neoplasm - metabolismen_HK
dc.subject.meshTransfectionen_HK
dc.subject.meshVascular Endothelial Growth Factor Aen_HK
dc.subject.meshVascular Endothelial Growth Factorsen_HK
dc.titleMacrophage migration inhibitory factor: Roles in regulating tumor cell migration and expression of angiogenic factors in hepatocellular carcinomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0020-7136&volume=107&issue=1&spage=22&epage=29&date=2003&atitle=Macrophage+migration+inhibitory+factor:+roles+in+regulating+tumor+cell+migration+and+expression+of+angiogenic+factors+in+hepatocellular+carcinomaen_HK
dc.identifier.emailPoon, RTP: poontp@hkucc.hku.hken_HK
dc.identifier.emailNg, IOL: iolng@hkucc.hku.hken_HK
dc.identifier.emailFan, ST: stfan@hku.hken_HK
dc.identifier.authorityPoon, RTP=rp00446en_HK
dc.identifier.authorityNg, IOL=rp00335en_HK
dc.identifier.authorityFan, ST=rp00355en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/ijc.11287en_HK
dc.identifier.pmid12925952-
dc.identifier.scopuseid_2-s2.0-0041413019en_HK
dc.identifier.hkuros83306en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0041413019&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume107en_HK
dc.identifier.issue1en_HK
dc.identifier.spage22en_HK
dc.identifier.epage29en_HK
dc.identifier.isiWOS:000185244300003-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridRen, Y=8109150500en_HK
dc.identifier.scopusauthoridTsui, HT=7006596183en_HK
dc.identifier.scopusauthoridPoon, RTP=7103097223en_HK
dc.identifier.scopusauthoridNg, IOL=7102753722en_HK
dc.identifier.scopusauthoridLi, Z=36064156900en_HK
dc.identifier.scopusauthoridChen, Y=16416830300en_HK
dc.identifier.scopusauthoridJiang, G=47061471400en_HK
dc.identifier.scopusauthoridLau, C=8086563300en_HK
dc.identifier.scopusauthoridYu, WC=24490445800en_HK
dc.identifier.scopusauthoridBacher, M=7006830551en_HK
dc.identifier.scopusauthoridFan, ST=7402678224en_HK

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