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Article: Progressive changes in Met-dependent signaling in a human ovarian surface epithelial model of malignant transformation

TitleProgressive changes in Met-dependent signaling in a human ovarian surface epithelial model of malignant transformation
Authors
KeywordsCell motility
Hepatocyte growth factor
Hepatocyte growth factor receptor
Human ovarian surface epithelium
Invasion
Met oncogene
Ovarian cancer
Issue Date2004
PublisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexcr
Citation
Experimental Cell Research, 2004, v. 299 n. 1, p. 248-256 How to Cite?
AbstractWe used an experimental in vitro model of human ovarian surface epithelium (OSE), the tissue of origin of >90% of ovarian cancers, to more precisely define the contribution of hepatocyte growth factor (HGF) to various OSE phenotypes at different stages of neoplastic progression. Neoplastic transformation of OSE in cultures was achieved by multiple genetic manipulations, resulting in the nontumorigenic line IOSE-29, the tumorigenic IOSE-Ov29, and the tumor-derived, more highly malignant IOSE-Ov29/T4. We demonstrate here that, compared to IOSE-29, IOSE-Ov29 and IOSE-Ov29/T4 exhibited higher levels of the HGF receptor Met and an increasing duration of ERK1/2 activation with malignant progression, in conjunction with other neoplastic properties. HGF activated Met signaling in all lines but elicited different responses: HGF induced cell dispersion (scattering) and collagen gel invasion in IOSE-Ov29 and IOSE-Ov29/T4 but did not alter the growth pattern of IOSE-29. Inhibition with PD98059 and LY294002 independently prevented HGF-induced invasive growth. Furthermore, our results show that HGF-induced invasion can be mediated through a rapamycin-sensitive p70 S6K cascade, which demonstrates that p70S6K can regulate cell motility in addition to its well-established role in protein synthesis. Taken together, our data correlate specific responses to HGF-mediated signaling with specific signaling pathways and with progressive neoplastic changes. © 2004 Elsevier Inc. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/84857
ISSN
2015 Impact Factor: 3.378
2015 SCImago Journal Rankings: 1.900
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWong, ASTen_HK
dc.contributor.authorRoskelley, CDen_HK
dc.contributor.authorPelech, Sen_HK
dc.contributor.authorMiller, Den_HK
dc.contributor.authorLeung, PCKen_HK
dc.contributor.authorAuersperg, Nen_HK
dc.date.accessioned2010-09-06T08:57:56Z-
dc.date.available2010-09-06T08:57:56Z-
dc.date.issued2004en_HK
dc.identifier.citationExperimental Cell Research, 2004, v. 299 n. 1, p. 248-256en_HK
dc.identifier.issn0014-4827en_HK
dc.identifier.urihttp://hdl.handle.net/10722/84857-
dc.description.abstractWe used an experimental in vitro model of human ovarian surface epithelium (OSE), the tissue of origin of >90% of ovarian cancers, to more precisely define the contribution of hepatocyte growth factor (HGF) to various OSE phenotypes at different stages of neoplastic progression. Neoplastic transformation of OSE in cultures was achieved by multiple genetic manipulations, resulting in the nontumorigenic line IOSE-29, the tumorigenic IOSE-Ov29, and the tumor-derived, more highly malignant IOSE-Ov29/T4. We demonstrate here that, compared to IOSE-29, IOSE-Ov29 and IOSE-Ov29/T4 exhibited higher levels of the HGF receptor Met and an increasing duration of ERK1/2 activation with malignant progression, in conjunction with other neoplastic properties. HGF activated Met signaling in all lines but elicited different responses: HGF induced cell dispersion (scattering) and collagen gel invasion in IOSE-Ov29 and IOSE-Ov29/T4 but did not alter the growth pattern of IOSE-29. Inhibition with PD98059 and LY294002 independently prevented HGF-induced invasive growth. Furthermore, our results show that HGF-induced invasion can be mediated through a rapamycin-sensitive p70 S6K cascade, which demonstrates that p70S6K can regulate cell motility in addition to its well-established role in protein synthesis. Taken together, our data correlate specific responses to HGF-mediated signaling with specific signaling pathways and with progressive neoplastic changes. © 2004 Elsevier Inc. All rights reserved.en_HK
dc.languageengen_HK
dc.publisherAcademic Press. The Journal's web site is located at http://www.elsevier.com/locate/yexcren_HK
dc.relation.ispartofExperimental Cell Researchen_HK
dc.subjectCell motilityen_HK
dc.subjectHepatocyte growth factoren_HK
dc.subjectHepatocyte growth factor receptoren_HK
dc.subjectHuman ovarian surface epitheliumen_HK
dc.subjectInvasionen_HK
dc.subjectMet oncogeneen_HK
dc.subjectOvarian canceren_HK
dc.titleProgressive changes in Met-dependent signaling in a human ovarian surface epithelial model of malignant transformationen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0014-4827&volume=299&spage=248&epage=256&date=2004&atitle=Progressive+changes+in+Met-dependent+signaling+in+a+human+ovarian+surface+epithelial+model+of+malignant+transformationen_HK
dc.identifier.emailWong, AST: awong1@hkucc.hku.hken_HK
dc.identifier.authorityWong, AST=rp00805en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.yexcr.2004.06.002en_HK
dc.identifier.pmid15302591-
dc.identifier.scopuseid_2-s2.0-4043054354en_HK
dc.identifier.hkuros91122en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-4043054354&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume299en_HK
dc.identifier.issue1en_HK
dc.identifier.spage248en_HK
dc.identifier.epage256en_HK
dc.identifier.isiWOS:000223453400024-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridWong, AST=23987963300en_HK
dc.identifier.scopusauthoridRoskelley, CD=7004526388en_HK
dc.identifier.scopusauthoridPelech, S=19435899100en_HK
dc.identifier.scopusauthoridMiller, D=7407283902en_HK
dc.identifier.scopusauthoridLeung, PCK=55419381000en_HK
dc.identifier.scopusauthoridAuersperg, N=7006582556en_HK

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