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dc.creatorFiorio, E
dc.creatorMercanti, A
dc.creatorTerrasi, M
dc.creatorMicciolo, R
dc.creatorRemo, A
dc.creatorAuriemma, A
dc.creatorMolino, A
dc.creatorParolin, V
dc.creatorDi Stefano, B
dc.creatorBonetti, F
dc.creatorGiordano, A
dc.creatorCetto, GL
dc.creatorSurmacz, E
dc.date.accessioned2021-02-01T21:53:14Z
dc.date.available2021-02-01T21:53:14Z
dc.date.issued2008-10-22
dc.identifier.issn1471-2407
dc.identifier.issn1471-2407
dc.identifier.doihttp://dx.doi.org/10.34944/dspace/5581
dc.identifier.other18945363 (pubmed)
dc.identifier.urihttp://hdl.handle.net/20.500.12613/5599
dc.description.abstractBackground: Obesity in postmenopausal women is associated with increased breast cancer risk, development of more aggressive tumors and resistance to certain anti-breast cancer treatments. Some of these effects might be mediated by obesity hormone leptin, acting independently or modulating other signaling pathways. Here we focused on the link between leptin and HER2. We tested if HER2 and the leptin receptor (ObR) can be coexpressed in breast cancer cell models, whether these two receptors can physically interact, and whether leptin can transactivate HER2. Next, we studied if leptin/ObR can coexist with HER2 in breast cancer tissues, and if presence of these two systems correlates with specific clinicopathological features. Methods: Expression of ObR, HER2, phospo-HER2 was assessed by immonoblotting. Physical interactions between ObR and HER2 were probed by immunoprecipitation and fluorescent immunostaining. Expression of leptin and ObR in breast cancer tissues was detected by immunohistochemistry (IHC). Associations among markers studied by IHC were evaluated using Fisher's exact test for count data. Results: HER2 and ObR were coexpressed in all studied breast cancer cell lines. In MCF-7 cells, HER2 physically interacted with ObR and leptin treatment increased HER2 phosphorylation on Tyr 1248. In 59 breast cancers, the presence of leptin was correlated with ObR (the overall association was about 93%). This result was confirmed both in HER2-positive and in HER2-negative subgroups. The expression of leptin or ObR was numerically more frequent in larger (> 10 mm) tumors. Conclusion: Coexpression of HER2 and the leptin/ObR system might contribute to enhanced HER2 activity and reduced sensitivity to anti-HER2 treatments. © 2008 Fiorio et al; licensee BioMed Central Ltd.
dc.format.extent305-
dc.language.isoen
dc.relation.haspartBMC Cancer
dc.relation.isreferencedbySpringer Science and Business Media LLC
dc.rightsCC BY
dc.subjectBreast Neoplasms
dc.subjectCarcinoma, Ductal, Breast
dc.subjectCell Line, Tumor
dc.subjectFemale
dc.subjectGene Expression Regulation, Neoplastic
dc.subjectHumans
dc.subjectImmunohistochemistry
dc.subjectLeptin
dc.subjectObesity
dc.subjectPostmenopause
dc.subjectProtein Binding
dc.subjectReceptor Cross-Talk
dc.subjectReceptor, ErbB-2
dc.subjectReceptors, Leptin
dc.subjectRisk Factors
dc.subjectTranscriptional Activation
dc.titleLeptin/HER2 crosstalk in breast cancer: In vitro study and preliminary in vivo analysis
dc.typeArticle
dc.type.genreJournal Article
dc.relation.doi10.1186/1471-2407-8-305
dc.ada.noteFor Americans with Disabilities Act (ADA) accommodation, including help with reading this content, please contact scholarshare@temple.edu
dc.creator.orcidGiordano, Antonio|0000-0002-5959-016X
dc.date.updated2021-02-01T21:53:10Z
refterms.dateFOA2021-02-01T21:53:14Z


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