File Download
  • No File Attached
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Glial cell line-derived neurotrophic factor induces cell migration and matrix metalloproteinase-13 expression in glioma cells
  • Basic View
  • Metadata View
  • XML View
TitleGlial cell line-derived neurotrophic factor induces cell migration and matrix metalloproteinase-13 expression in glioma cells
 
AuthorsLu, DY2
Leung, YM2
Cheung, CW1
Chen, YR2
Wong, KL1 3
 
KeywordsAP-1
C-Jun
GDNF
Migration
MMP-13
 
Issue Date2010
 
PublisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharm
 
CitationBiochemical Pharmacology, 2010, v. 80 n. 8, p. 1201-1209 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.bcp.2010.06.046
 
AbstractMalignant gliomas are the most common primary brain tumors in adults and the second most common tumor in children. Gliomas are associated high morbidity and mortality because these tumors are highly invasive into surrounding brain tissue, making complete surgical resection impossible. Glial cell line-derived neurotrophic factor (GDNF) has been identified as a potent neurotrophic factor in a variety of neuronal cell populations. However, the molecular mechanisms and pathologic roles underlying GDNF-induced glioma migration remain unclear. In this study, we found that application of recombinant human GDNF enhances the migration of U87 and U251 cells but not C6 cells. In addition, we found that the expression of matrix metalloproteinase-13 (MMP-13) mRNA, protein and secretion increase in response to GDNF stimulation. The GDNF-induced increase in cell migration was antagonized by MMP-13 neutralizing antibody or silencing MMP-13. We then examined the involvement of mitogen-activated protein kinases (MAPKs) in glioma cell migration induced by GDNF. GDNF-induced MMP-13 expression and glioma migration were attenuated by MEK/extracellular signal-regulating kinase (ERK) and c-Jun N-terminal protein kinase (JNK) inhibitors, as well as ERK and JNK dominant-negative mutants. Treatment with GDNF-induced MEK/ERK and JNK/c-Jun activation and increased AP-1 DNA binding activity in a time-dependent manner. Treatment with AP-1 inhibitors (tanshinone IIA and curcumin) also reduced GDNF-induced glioma cell migration. In migration-prone sublines, cells with greater migration ability had higher GDNF expression. These results indicate that GDNF enhances migration of glioma cells through the increase of MMP-13 production and is mainly regulated by the MEK/ERK and JNK, c-Jun and AP-1 pathways. © 2010 Elsevier Inc.
 
ISSN0006-2952
2012 Impact Factor: 4.576
2012 SCImago Journal Rankings: 1.515
 
DOIhttp://dx.doi.org/10.1016/j.bcp.2010.06.046
 
ISI Accession Number IDWOS:000281936800010
Funding AgencyGrant Number
National Science CouncilNSC 98-2320-B-039-009-MY2
NSC 98-2627-B-039-005-
China Medical UniversityCMU98-N1-29
CMU98-C-14
Funding Information:

This work was supported by grants from the National Science Council (NSC 98-2320-B-039-009-MY2 and NSC 98-2627-B-039-005-) and China Medical University (CMU98-N1-29 and CMU98-C-14).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorLu, DY
 
dc.contributor.authorLeung, YM
 
dc.contributor.authorCheung, CW
 
dc.contributor.authorChen, YR
 
dc.contributor.authorWong, KL
 
dc.date.accessioned2011-04-04T02:32:49Z
 
dc.date.available2011-04-04T02:32:49Z
 
dc.date.issued2010
 
dc.description.abstractMalignant gliomas are the most common primary brain tumors in adults and the second most common tumor in children. Gliomas are associated high morbidity and mortality because these tumors are highly invasive into surrounding brain tissue, making complete surgical resection impossible. Glial cell line-derived neurotrophic factor (GDNF) has been identified as a potent neurotrophic factor in a variety of neuronal cell populations. However, the molecular mechanisms and pathologic roles underlying GDNF-induced glioma migration remain unclear. In this study, we found that application of recombinant human GDNF enhances the migration of U87 and U251 cells but not C6 cells. In addition, we found that the expression of matrix metalloproteinase-13 (MMP-13) mRNA, protein and secretion increase in response to GDNF stimulation. The GDNF-induced increase in cell migration was antagonized by MMP-13 neutralizing antibody or silencing MMP-13. We then examined the involvement of mitogen-activated protein kinases (MAPKs) in glioma cell migration induced by GDNF. GDNF-induced MMP-13 expression and glioma migration were attenuated by MEK/extracellular signal-regulating kinase (ERK) and c-Jun N-terminal protein kinase (JNK) inhibitors, as well as ERK and JNK dominant-negative mutants. Treatment with GDNF-induced MEK/ERK and JNK/c-Jun activation and increased AP-1 DNA binding activity in a time-dependent manner. Treatment with AP-1 inhibitors (tanshinone IIA and curcumin) also reduced GDNF-induced glioma cell migration. In migration-prone sublines, cells with greater migration ability had higher GDNF expression. These results indicate that GDNF enhances migration of glioma cells through the increase of MMP-13 production and is mainly regulated by the MEK/ERK and JNK, c-Jun and AP-1 pathways. © 2010 Elsevier Inc.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationBiochemical Pharmacology, 2010, v. 80 n. 8, p. 1201-1209 [How to Cite?]
DOI: http://dx.doi.org/10.1016/j.bcp.2010.06.046
 
dc.identifier.citeulike7480630
 
dc.identifier.doihttp://dx.doi.org/10.1016/j.bcp.2010.06.046
 
dc.identifier.epage1209
 
dc.identifier.hkuros183244
 
dc.identifier.isiWOS:000281936800010
Funding AgencyGrant Number
National Science CouncilNSC 98-2320-B-039-009-MY2
NSC 98-2627-B-039-005-
China Medical UniversityCMU98-N1-29
CMU98-C-14
Funding Information:

This work was supported by grants from the National Science Council (NSC 98-2320-B-039-009-MY2 and NSC 98-2627-B-039-005-) and China Medical University (CMU98-N1-29 and CMU98-C-14).

 
dc.identifier.issn0006-2952
2012 Impact Factor: 4.576
2012 SCImago Journal Rankings: 1.515
 
dc.identifier.issue8
 
dc.identifier.openurl
 
dc.identifier.pmid20615395
 
dc.identifier.scopuseid_2-s2.0-77956226027
 
dc.identifier.spage1201
 
dc.identifier.urihttp://hdl.handle.net/10722/132843
 
dc.identifier.volume80
 
dc.languageeng
 
dc.publisherElsevier Inc. The Journal's web site is located at http://www.elsevier.com/locate/biochempharm
 
dc.publisher.placeUnited States
 
dc.relation.ispartofBiochemical Pharmacology
 
dc.relation.referencesReferences in Scopus
 
dc.subject.meshExtracellular Signal-Regulated MAP Kinases - genetics - metabolism
 
dc.subject.meshGene Expression Regulation, Enzymologic - drug effects
 
dc.subject.meshGlial Cell Line-Derived Neurotrophic Factor - metabolism - pharmacology
 
dc.subject.meshMatrix Metalloproteinase 13 - genetics - metabolism
 
dc.subject.meshNeuroglia - drug effects - physiology
 
dc.subjectAP-1
 
dc.subjectC-Jun
 
dc.subjectGDNF
 
dc.subjectMigration
 
dc.subjectMMP-13
 
dc.titleGlial cell line-derived neurotrophic factor induces cell migration and matrix metalloproteinase-13 expression in glioma cells
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Lu, DY</contributor.author>
<contributor.author>Leung, YM</contributor.author>
<contributor.author>Cheung, CW</contributor.author>
<contributor.author>Chen, YR</contributor.author>
<contributor.author>Wong, KL</contributor.author>
<date.accessioned>2011-04-04T02:32:49Z</date.accessioned>
<date.available>2011-04-04T02:32:49Z</date.available>
<date.issued>2010</date.issued>
<identifier.citation>Biochemical Pharmacology, 2010, v. 80 n. 8, p. 1201-1209</identifier.citation>
<identifier.issn>0006-2952</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/132843</identifier.uri>
<description.abstract>Malignant gliomas are the most common primary brain tumors in adults and the second most common tumor in children. Gliomas are associated high morbidity and mortality because these tumors are highly invasive into surrounding brain tissue, making complete surgical resection impossible. Glial cell line-derived neurotrophic factor (GDNF) has been identified as a potent neurotrophic factor in a variety of neuronal cell populations. However, the molecular mechanisms and pathologic roles underlying GDNF-induced glioma migration remain unclear. In this study, we found that application of recombinant human GDNF enhances the migration of U87 and U251 cells but not C6 cells. In addition, we found that the expression of matrix metalloproteinase-13 (MMP-13) mRNA, protein and secretion increase in response to GDNF stimulation. The GDNF-induced increase in cell migration was antagonized by MMP-13 neutralizing antibody or silencing MMP-13. We then examined the involvement of mitogen-activated protein kinases (MAPKs) in glioma cell migration induced by GDNF. GDNF-induced MMP-13 expression and glioma migration were attenuated by MEK/extracellular signal-regulating kinase (ERK) and c-Jun N-terminal protein kinase (JNK) inhibitors, as well as ERK and JNK dominant-negative mutants. Treatment with GDNF-induced MEK/ERK and JNK/c-Jun activation and increased AP-1 DNA binding activity in a time-dependent manner. Treatment with AP-1 inhibitors (tanshinone IIA and curcumin) also reduced GDNF-induced glioma cell migration. In migration-prone sublines, cells with greater migration ability had higher GDNF expression. These results indicate that GDNF enhances migration of glioma cells through the increase of MMP-13 production and is mainly regulated by the MEK/ERK and JNK, c-Jun and AP-1 pathways. &#169; 2010 Elsevier Inc.</description.abstract>
<language>eng</language>
<publisher>Elsevier Inc. The Journal&apos;s web site is located at http://www.elsevier.com/locate/biochempharm</publisher>
<relation.ispartof>Biochemical Pharmacology</relation.ispartof>
<subject>AP-1</subject>
<subject>C-Jun</subject>
<subject>GDNF</subject>
<subject>Migration</subject>
<subject>MMP-13</subject>
<subject.mesh>Extracellular Signal-Regulated MAP Kinases - genetics - metabolism</subject.mesh>
<subject.mesh>Gene Expression Regulation, Enzymologic - drug effects</subject.mesh>
<subject.mesh>Glial Cell Line-Derived Neurotrophic Factor - metabolism - pharmacology</subject.mesh>
<subject.mesh>Matrix Metalloproteinase 13 - genetics - metabolism</subject.mesh>
<subject.mesh>Neuroglia - drug effects - physiology</subject.mesh>
<title>Glial cell line-derived neurotrophic factor induces cell migration and matrix metalloproteinase-13 expression in glioma cells</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=0006-2952&amp;volume=80&amp;issue=8&amp;spage=1201&amp;epage=1209&amp;date=2010&amp;atitle=Glial+cell+line-derived+neurotrophic+factor+induces+cell+migration+and+matrix+metalloproteinase-13+expression+in+glioma+cells</identifier.openurl>
<description.nature>Link_to_subscribed_fulltext</description.nature>
<identifier.doi>10.1016/j.bcp.2010.06.046</identifier.doi>
<identifier.pmid>20615395</identifier.pmid>
<identifier.scopus>eid_2-s2.0-77956226027</identifier.scopus>
<identifier.hkuros>183244</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-77956226027&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>80</identifier.volume>
<identifier.issue>8</identifier.issue>
<identifier.spage>1201</identifier.spage>
<identifier.epage>1209</identifier.epage>
<identifier.isi>WOS:000281936800010</identifier.isi>
<publisher.place>United States</publisher.place>
<identifier.citeulike>7480630</identifier.citeulike>
</item>
Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine
  2. null
  3. China Medical University Hospital Taichung