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Article: Upregulation of macrophage migration inhibitory factor contributes to induced N-Myc expression by the activation of ERK signaling pathway and increased expression of interleukin-8 and VEGF in neuroblastoma

TitleUpregulation of macrophage migration inhibitory factor contributes to induced N-Myc expression by the activation of ERK signaling pathway and increased expression of interleukin-8 and VEGF in neuroblastoma
Authors
KeywordsAngiogenesis
MAPK
MIF
N-myc
Neuroblastoma
Issue Date2004
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/onc
Citation
Oncogene, 2004, v. 23 n. 23, p. 4146-4154 How to Cite?
AbstractMacrophage migration inhibitory factor (MIF) has been linked to fundamental processes such as control of cell proliferation, cell survival, angiogenesis, and tumor progression. The expression of MIF has been reported in several tumors. However, the precise role of MIF in tumor cells remains unclear. In the present study, we investigated the expression pattern and the function of MIF in neuroblastoma. Our results showed that intracellular MIF was upregulated in neuroblastoma tumor tissues and cell lines. MIF protein expression significantly correlated with the grade of tumor differentiation. In addition, we found that MIF induced a significant close-dependent increase of vascular endothelial growth factor and interleukin-8 secretion. We also observed that an increased MIF expression level correlated with N-Myc protein (the N-myc oncogene product) expression in neuroblastoma tissues. MIF increased the expression of N-myc mRNA and N-Myc protein and induced N-Myc translocation from the cytoplasm to nucleus in neuroblastoma cell lines. MIF-induced N-Myc expression was found to be dependent on ERK signaling pathways. The inhibition of ERK activation reduced MIF-mediated N-Myc expression. These results suggest that MIF may contribute to the progression of neuroblastoma by (a) inducing N-Myc expression and (b) upregulating the expression of angiogenic factors.
Persistent Identifierhttp://hdl.handle.net/10722/88282
ISSN
2015 Impact Factor: 7.932
2015 SCImago Journal Rankings: 4.047
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorRen, Yen_HK
dc.contributor.authorChan, HMen_HK
dc.contributor.authorLi, Zen_HK
dc.contributor.authorLin, Cen_HK
dc.contributor.authorNicholls, Jen_HK
dc.contributor.authorChen, CFen_HK
dc.contributor.authorLee, PYen_HK
dc.contributor.authorLui, Ven_HK
dc.contributor.authorBacher, Men_HK
dc.contributor.authorTam, PKHen_HK
dc.date.accessioned2010-09-06T09:41:19Z-
dc.date.available2010-09-06T09:41:19Z-
dc.date.issued2004en_HK
dc.identifier.citationOncogene, 2004, v. 23 n. 23, p. 4146-4154en_HK
dc.identifier.issn0950-9232en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88282-
dc.description.abstractMacrophage migration inhibitory factor (MIF) has been linked to fundamental processes such as control of cell proliferation, cell survival, angiogenesis, and tumor progression. The expression of MIF has been reported in several tumors. However, the precise role of MIF in tumor cells remains unclear. In the present study, we investigated the expression pattern and the function of MIF in neuroblastoma. Our results showed that intracellular MIF was upregulated in neuroblastoma tumor tissues and cell lines. MIF protein expression significantly correlated with the grade of tumor differentiation. In addition, we found that MIF induced a significant close-dependent increase of vascular endothelial growth factor and interleukin-8 secretion. We also observed that an increased MIF expression level correlated with N-Myc protein (the N-myc oncogene product) expression in neuroblastoma tissues. MIF increased the expression of N-myc mRNA and N-Myc protein and induced N-Myc translocation from the cytoplasm to nucleus in neuroblastoma cell lines. MIF-induced N-Myc expression was found to be dependent on ERK signaling pathways. The inhibition of ERK activation reduced MIF-mediated N-Myc expression. These results suggest that MIF may contribute to the progression of neuroblastoma by (a) inducing N-Myc expression and (b) upregulating the expression of angiogenic factors.en_HK
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/oncen_HK
dc.relation.ispartofOncogeneen_HK
dc.subjectAngiogenesisen_HK
dc.subjectMAPKen_HK
dc.subjectMIFen_HK
dc.subjectN-mycen_HK
dc.subjectNeuroblastomaen_HK
dc.subject.meshAdolescenten_HK
dc.subject.meshAdulten_HK
dc.subject.meshChilden_HK
dc.subject.meshChild, Preschoolen_HK
dc.subject.meshDown-Regulationen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshHumansen_HK
dc.subject.meshInfanten_HK
dc.subject.meshInterleukin-8 - biosynthesis - geneticsen_HK
dc.subject.meshMacrophage Migration-Inhibitory Factors - metabolismen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMitogen-Activated Protein Kinases - antagonists & inhibitors - metabolismen_HK
dc.subject.meshNeuroblastoma - metabolism - pathologyen_HK
dc.subject.meshProto-Oncogene Proteins c-myc - biosynthesis - geneticsen_HK
dc.subject.meshUp-Regulationen_HK
dc.subject.meshVascular Endothelial Growth Factor A - biosynthesis - geneticsen_HK
dc.titleUpregulation of macrophage migration inhibitory factor contributes to induced N-Myc expression by the activation of ERK signaling pathway and increased expression of interleukin-8 and VEGF in neuroblastomaen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0950-9232&volume=23&spage=4146&epage=4154&date=2004&atitle=Upregulation+of+macrophage+migration+inhibitory+factor+contributes+to+induced+N-Myc+expression+by+the+activation+of+ERK+signaling+pathway+and+increased+expression+of+interleukin-8+and+VEGF+in+neuroblastomaen_HK
dc.identifier.emailNicholls, J: nicholls@pathology.hku.hken_HK
dc.identifier.emailLui, V: vchlui@hkucc.hku.hken_HK
dc.identifier.emailTam, PKH: paultam@hkucc.hku.hken_HK
dc.identifier.authorityNicholls, J=rp00364en_HK
dc.identifier.authorityLui, V=rp00363en_HK
dc.identifier.authorityTam, PKH=rp00060en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1038/sj.onc.1207490en_HK
dc.identifier.pmid15064733-
dc.identifier.scopuseid_2-s2.0-2942593696en_HK
dc.identifier.hkuros85956en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-2942593696&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume23en_HK
dc.identifier.issue23en_HK
dc.identifier.spage4146en_HK
dc.identifier.epage4154en_HK
dc.identifier.isiWOS:000221520200013-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridRen, Y=8109150500en_HK
dc.identifier.scopusauthoridChan, HM=7403402552en_HK
dc.identifier.scopusauthoridLi, Z=36064156900en_HK
dc.identifier.scopusauthoridLin, C=27169299500en_HK
dc.identifier.scopusauthoridNicholls, J=7201463077en_HK
dc.identifier.scopusauthoridChen, CF=7501960390en_HK
dc.identifier.scopusauthoridLee, PY=37056368600en_HK
dc.identifier.scopusauthoridLui, V=7004231344en_HK
dc.identifier.scopusauthoridBacher, M=7006830551en_HK
dc.identifier.scopusauthoridTam, PKH=7202539421en_HK

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