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Article: FTY720, a fungus metabolite, inhibits invasion ability of androgen-independent prostate cancer cells through inactivation of RhoA-GTPase

TitleFTY720, a fungus metabolite, inhibits invasion ability of androgen-independent prostate cancer cells through inactivation of RhoA-GTPase
Authors
KeywordsFTY720
Invasion
Prostate cancer
RhoA
Issue Date2006
PublisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canlet
Citation
Cancer Letters, 2006, v. 233 n. 1, p. 36-47 How to Cite?
AbstractThe failure of controlling androgen-independent and metastatic prostate cancer growth is the main cause of death in prostate cancer patients. In this study, we have demonstrated evidence on the inhibitory effects of a fungus metabolite, FTY720, on the clonogenesity as well as invasion ability of androgen-independent prostate cancer cells. First, using colony forming assay, we found that FTY720 treatment led to decreased colony forming ability of androgen-independent prostate cancer cell lines DU145 and PC3, indicating its negative role on cancer cell survival. In addition, treatment with relatively low dose of FTY720 (i.e. inhibitory concentration of 50% cell survival) resulted in suppression of prostate cancer cell migration and invasion abilities demonstrated by Wound closure, 3D collagen gel invasion assays and stress fiber staining. Furthermore, we found that the inhibitory effect of FTY720 on prostate cancer invasion was associated with down-regulation of GTP-bound active form of RhoA. Transfection of a dominant-active RhoA vector in DU145 and PC3 cells conferred resistance to FTY720. Since activation of RhoA-GTPase is associated with metastasis in many types of malignancies, our results not only suggest a new agent for the treatment of advanced prostate cancer, but also implicate a possible novel anticancer drug especially against metastatic cancers. © 2005 Elsevier Ireland Ltd. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67345
ISSN
2015 Impact Factor: 5.992
2015 SCImago Journal Rankings: 2.331
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorZhou, Cen_HK
dc.contributor.authorLing, MTen_HK
dc.contributor.authorKinWah Lee, Ten_HK
dc.contributor.authorMan, Ken_HK
dc.contributor.authorWang, Xen_HK
dc.contributor.authorWong, YCen_HK
dc.date.accessioned2010-09-06T05:54:18Z-
dc.date.available2010-09-06T05:54:18Z-
dc.date.issued2006en_HK
dc.identifier.citationCancer Letters, 2006, v. 233 n. 1, p. 36-47en_HK
dc.identifier.issn0304-3835en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67345-
dc.description.abstractThe failure of controlling androgen-independent and metastatic prostate cancer growth is the main cause of death in prostate cancer patients. In this study, we have demonstrated evidence on the inhibitory effects of a fungus metabolite, FTY720, on the clonogenesity as well as invasion ability of androgen-independent prostate cancer cells. First, using colony forming assay, we found that FTY720 treatment led to decreased colony forming ability of androgen-independent prostate cancer cell lines DU145 and PC3, indicating its negative role on cancer cell survival. In addition, treatment with relatively low dose of FTY720 (i.e. inhibitory concentration of 50% cell survival) resulted in suppression of prostate cancer cell migration and invasion abilities demonstrated by Wound closure, 3D collagen gel invasion assays and stress fiber staining. Furthermore, we found that the inhibitory effect of FTY720 on prostate cancer invasion was associated with down-regulation of GTP-bound active form of RhoA. Transfection of a dominant-active RhoA vector in DU145 and PC3 cells conferred resistance to FTY720. Since activation of RhoA-GTPase is associated with metastasis in many types of malignancies, our results not only suggest a new agent for the treatment of advanced prostate cancer, but also implicate a possible novel anticancer drug especially against metastatic cancers. © 2005 Elsevier Ireland Ltd. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherElsevier Ireland Ltd. The Journal's web site is located at http://www.elsevier.com/locate/canleten_HK
dc.relation.ispartofCancer Lettersen_HK
dc.rightsCancer Letters. Copyright © Elsevier Ireland Ltd.en_HK
dc.subjectFTY720en_HK
dc.subjectInvasionen_HK
dc.subjectProstate canceren_HK
dc.subjectRhoAen_HK
dc.subject.meshAntineoplastic Agents - pharmacologyen_HK
dc.subject.meshCell Line, Tumoren_HK
dc.subject.meshCell Movement - drug effectsen_HK
dc.subject.meshCytoskeleton - drug effectsen_HK
dc.subject.meshHumansen_HK
dc.subject.meshMaleen_HK
dc.subject.meshNeoplasm Invasivenessen_HK
dc.subject.meshPropylene Glycols - pharmacologyen_HK
dc.subject.meshProstatic Neoplasms - drug therapy - enzymology - pathologyen_HK
dc.subject.meshSphingosine - analogs & derivatives - pharmacologyen_HK
dc.subject.meshrhoA GTP-Binding Protein - antagonists & inhibitorsen_HK
dc.titleFTY720, a fungus metabolite, inhibits invasion ability of androgen-independent prostate cancer cells through inactivation of RhoA-GTPaseen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0304-3835&volume=233&spage=36&epage=47&date=2006&atitle=FTY720,+a+fungus+metabolite,+inhibits+invasion+ability+of+androgen-independent+prostate+cancer+cells+through+inactivation+of+RhoA-GTPaseen_HK
dc.identifier.emailLing, MT: patling@hkucc.hku.hken_HK
dc.identifier.emailMan, K: kwanman@hkucc.hku.hken_HK
dc.identifier.emailWong, YC: ycwong@hkucc.hku.hken_HK
dc.identifier.authorityLing, MT=rp00449en_HK
dc.identifier.authorityMan, K=rp00417en_HK
dc.identifier.authorityWong, YC=rp00316en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.canlet.2005.02.039en_HK
dc.identifier.pmid16473668-
dc.identifier.scopuseid_2-s2.0-32244448999en_HK
dc.identifier.hkuros115049en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-32244448999&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume233en_HK
dc.identifier.issue1en_HK
dc.identifier.spage36en_HK
dc.identifier.epage47en_HK
dc.identifier.isiWOS:000235851300006-
dc.publisher.placeIrelanden_HK
dc.identifier.scopusauthoridZhou, C=55245030500en_HK
dc.identifier.scopusauthoridLing, MT=7102229780en_HK
dc.identifier.scopusauthoridKinWah Lee, T=12240167500en_HK
dc.identifier.scopusauthoridMan, K=7101754072en_HK
dc.identifier.scopusauthoridWang, X=7501854829en_HK
dc.identifier.scopusauthoridWong, YC=7403041798en_HK

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