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Article: Gonadotropin-releasing hormone: GnRH receptor signaling in extrapituitary tissues

TitleGonadotropin-releasing hormone: GnRH receptor signaling in extrapituitary tissues
Authors
KeywordsCross-talk
Extrapituitary
GnRH
GnRH receptor
MAPK
Metastasis
Pituitary
Receptor tyrosine kinase
Signaling
Tumor
Issue Date2008
PublisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.febsjournal.org/
Citation
Febs Journal, 2008, v. 275 n. 22, p. 5479-5495 How to Cite?
AbstractGonadotropin-releasing hormone (GnRH) has historically been known as a pituitary hormone; however, in the past few years, interest has been raised in locally produced, extrapituitary GnRH. GnRH receptor (GnRHR) was found to be expressed in normal human reproductive tissues (e.g. breast, endometrium, ovary, and prostate) and tumors derived from these tissues. Numerous studies have provided evidence for a role of GnRH in cell proliferation. More recently, we and others have reported a novel role for GnRH in other aspects of tumor progression, such as metastasis and angiogenesis. The multiple actions of GnRH could be linked to the divergence of signaling pathways that are activated by GnRHR. Recent observations also demonstrate cross-talk between GnRHR and growth factor receptors. Intriguingly, the classical Gαq-11- phospholipase C signal transduction pathway, known to function in pituitary gonadotropes, is not involved in GnRH actions at nonpituitary targets. Herein, we review the key findings on the role of GnRH in the control of tumor growth, progression, and dissemination. The emerging role of GnRHR in actin cytoskeleton remodeling (small Rho GTPases), expression and/or activity of adhesion molecules (integrins), proteolytic enzymes (matrix metalloproteinases) and angiogenic factors is explored. The signal transduction mechanisms of GnRHR in mediating these activities is described. Finally, we discuss how a common GnRHR may mediate different, even opposite, responses to GnRH in the same tissue/cell type and whether an additional receptor(s) for GnRH exists. © 2008 The Authors.
Persistent Identifierhttp://hdl.handle.net/10722/89269
ISSN
2015 Impact Factor: 4.237
2015 SCImago Journal Rankings: 2.141
ISI Accession Number ID
Funding AgencyGrant Number
Hong Kong Research Grant Council778108
Funding Information:

This work was supported by the Hong Kong Research Grant Council grant 778108 to A. S. T. Wong.

References

 

DC FieldValueLanguage
dc.contributor.authorCheung, LWTen_HK
dc.contributor.authorWong, ASTen_HK
dc.date.accessioned2010-09-06T09:54:42Z-
dc.date.available2010-09-06T09:54:42Z-
dc.date.issued2008en_HK
dc.identifier.citationFebs Journal, 2008, v. 275 n. 22, p. 5479-5495en_HK
dc.identifier.issn1742-464Xen_HK
dc.identifier.urihttp://hdl.handle.net/10722/89269-
dc.description.abstractGonadotropin-releasing hormone (GnRH) has historically been known as a pituitary hormone; however, in the past few years, interest has been raised in locally produced, extrapituitary GnRH. GnRH receptor (GnRHR) was found to be expressed in normal human reproductive tissues (e.g. breast, endometrium, ovary, and prostate) and tumors derived from these tissues. Numerous studies have provided evidence for a role of GnRH in cell proliferation. More recently, we and others have reported a novel role for GnRH in other aspects of tumor progression, such as metastasis and angiogenesis. The multiple actions of GnRH could be linked to the divergence of signaling pathways that are activated by GnRHR. Recent observations also demonstrate cross-talk between GnRHR and growth factor receptors. Intriguingly, the classical Gαq-11- phospholipase C signal transduction pathway, known to function in pituitary gonadotropes, is not involved in GnRH actions at nonpituitary targets. Herein, we review the key findings on the role of GnRH in the control of tumor growth, progression, and dissemination. The emerging role of GnRHR in actin cytoskeleton remodeling (small Rho GTPases), expression and/or activity of adhesion molecules (integrins), proteolytic enzymes (matrix metalloproteinases) and angiogenic factors is explored. The signal transduction mechanisms of GnRHR in mediating these activities is described. Finally, we discuss how a common GnRHR may mediate different, even opposite, responses to GnRH in the same tissue/cell type and whether an additional receptor(s) for GnRH exists. © 2008 The Authors.en_HK
dc.languageengen_HK
dc.publisherWiley-Blackwell Publishing Ltd.. The Journal's web site is located at http://www.febsjournal.org/en_HK
dc.relation.ispartofFEBS Journalen_HK
dc.rightsThe F E B S Journal. Copyright © Blackwell Publishing Ltd.en_HK
dc.subjectCross-talken_HK
dc.subjectExtrapituitaryen_HK
dc.subjectGnRHen_HK
dc.subjectGnRH receptoren_HK
dc.subjectMAPKen_HK
dc.subjectMetastasisen_HK
dc.subjectPituitaryen_HK
dc.subjectReceptor tyrosine kinaseen_HK
dc.subjectSignalingen_HK
dc.subjectTumoren_HK
dc.titleGonadotropin-releasing hormone: GnRH receptor signaling in extrapituitary tissuesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1742-464X&volume=275&spage=5479&epage=5495&date=2008&atitle=GnRH+receptor+signaling+in+extrapituitary+tissuesen_HK
dc.identifier.emailWong, AST: awong1@hkucc.hku.hken_HK
dc.identifier.authorityWong, AST=rp00805en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1111/j.1742-4658.2008.06677.xen_HK
dc.identifier.pmid18959738-
dc.identifier.scopuseid_2-s2.0-54849408590en_HK
dc.identifier.hkuros144167en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-54849408590&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume275en_HK
dc.identifier.issue22en_HK
dc.identifier.spage5479en_HK
dc.identifier.epage5495en_HK
dc.identifier.isiWOS:000260348600003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridCheung, LWT=14119560800en_HK
dc.identifier.scopusauthoridWong, AST=23987963300en_HK
dc.identifier.citeulike3454868-

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