File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Inducible expression of FGF-3 in mouse mammary gland

TitleInducible expression of FGF-3 in mouse mammary gland
Authors
Issue Date2002
PublisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.org
Citation
Proceedings Of The National Academy Of Sciences Of The United States Of America, 2002, v. 99 n. 17, p. 11187-11192 How to Cite?
AbstractFibroblast growth factor-3 (FGF-3) is a crucial developmental regulator. Aberrant activation of this gene by mouse mammary tumor virus insertion results in pregnancy-responsive mammary tumorigenesis. To characterize better FGF-3 function in postnatal mammary gland development and cancer initiation/progression, we used a mifepristone (RU486)-inducible regulatory system to express conditionally FGF-3 in the mammary epithelium of transgenic mice. Ectopic over-expression of FGF-3 in pubescent mammary glands elicited severe perturbations in early mammary gland development leading to mammary hyperplasia. Ductal elongation was retarded, multiple cysts persisted in the virgin ducts, and ductal epithelium was expanded and multilayered. The altered ductal architecture and the persistence of hyperplastic multilayered epithelium reflect a defect in growth regulation, which resulted from an imbalance between mitogenic and apoptotic signals. By altering the duration of RU486 treatment, we showed that the persistence of mitogenic signal elicited by FGF-3 is crucial for the initiation, progression, and maintenance of the hyperplastic characteristic of the mammary epithelium. The manifestations elicited by FGF-3 could be reversed by RU486 withdrawal. In addition, synergism between the stimulus from estrogen and FGF-3 mitogenic pathways was evident and likely contributes to the pregnancy-dependent tumorigenesis of FGF-3. Taken together, the mifepristone-inducible regulatory system provides a powerful means for understanding the diverse roles of FGF-3 and its interactions with hormones in mammary gland tumorigenesis.
Persistent Identifierhttp://hdl.handle.net/10722/172813
ISSN
2015 Impact Factor: 9.423
2015 SCImago Journal Rankings: 6.883
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorNgan, ESWen_US
dc.contributor.authorMa, ZQen_US
dc.contributor.authorChua, SSen_US
dc.contributor.authorDemayo, FJen_US
dc.contributor.authorTsai, SYen_US
dc.date.accessioned2012-10-30T06:25:03Z-
dc.date.available2012-10-30T06:25:03Z-
dc.date.issued2002en_US
dc.identifier.citationProceedings Of The National Academy Of Sciences Of The United States Of America, 2002, v. 99 n. 17, p. 11187-11192en_US
dc.identifier.issn0027-8424en_US
dc.identifier.urihttp://hdl.handle.net/10722/172813-
dc.description.abstractFibroblast growth factor-3 (FGF-3) is a crucial developmental regulator. Aberrant activation of this gene by mouse mammary tumor virus insertion results in pregnancy-responsive mammary tumorigenesis. To characterize better FGF-3 function in postnatal mammary gland development and cancer initiation/progression, we used a mifepristone (RU486)-inducible regulatory system to express conditionally FGF-3 in the mammary epithelium of transgenic mice. Ectopic over-expression of FGF-3 in pubescent mammary glands elicited severe perturbations in early mammary gland development leading to mammary hyperplasia. Ductal elongation was retarded, multiple cysts persisted in the virgin ducts, and ductal epithelium was expanded and multilayered. The altered ductal architecture and the persistence of hyperplastic multilayered epithelium reflect a defect in growth regulation, which resulted from an imbalance between mitogenic and apoptotic signals. By altering the duration of RU486 treatment, we showed that the persistence of mitogenic signal elicited by FGF-3 is crucial for the initiation, progression, and maintenance of the hyperplastic characteristic of the mammary epithelium. The manifestations elicited by FGF-3 could be reversed by RU486 withdrawal. In addition, synergism between the stimulus from estrogen and FGF-3 mitogenic pathways was evident and likely contributes to the pregnancy-dependent tumorigenesis of FGF-3. Taken together, the mifepristone-inducible regulatory system provides a powerful means for understanding the diverse roles of FGF-3 and its interactions with hormones in mammary gland tumorigenesis.en_US
dc.languageengen_US
dc.publisherNational Academy of Sciences. The Journal's web site is located at http://www.pnas.orgen_US
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of Americaen_US
dc.subject.meshAnimalsen_US
dc.subject.meshCell Adhesion Molecules - Geneticsen_US
dc.subject.meshDisease Progressionen_US
dc.subject.meshEpithelial Cells - Physiologyen_US
dc.subject.meshFemaleen_US
dc.subject.meshFibroblast Growth Factor 3en_US
dc.subject.meshFibroblast Growth Factors - Geneticsen_US
dc.subject.meshGene Expression Regulation, Developmental - Physiologyen_US
dc.subject.meshHyperplasiaen_US
dc.subject.meshMammary Glands, Animal - Drug Effects - Metabolism - Pathologyen_US
dc.subject.meshMammary Neoplasms, Animal - Genetics - Pathologyen_US
dc.subject.meshMiceen_US
dc.subject.meshMice, Transgenicen_US
dc.subject.meshMifepristone - Pharmacologyen_US
dc.subject.meshOvariectomyen_US
dc.subject.meshProto-Oncogene Proteins - Geneticsen_US
dc.subject.meshSexual Maturationen_US
dc.titleInducible expression of FGF-3 in mouse mammary glanden_US
dc.typeArticleen_US
dc.identifier.emailNgan, ESW: engan@hkucc.hku.hken_US
dc.identifier.authorityNgan, ESW=rp00422en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1073/pnas.172366199en_US
dc.identifier.pmid12169667-
dc.identifier.scopuseid_2-s2.0-0037143665en_US
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0037143665&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume99en_US
dc.identifier.issue17en_US
dc.identifier.spage11187en_US
dc.identifier.epage11192en_US
dc.identifier.isiWOS:000177606900044-
dc.publisher.placeUnited Statesen_US
dc.identifier.scopusauthoridNgan, ESW=22234827500en_US
dc.identifier.scopusauthoridMa, ZQ=7403600106en_US
dc.identifier.scopusauthoridChua, SS=7201550437en_US
dc.identifier.scopusauthoridDeMayo, FJ=7005462358en_US
dc.identifier.scopusauthoridTsai, SY=7403478781en_US
dc.identifier.citeulike9206882-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats