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    Leptin/HER2 crosstalk in breast cancer: In vitro study and preliminary in vivo analysis

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    Name:
    LeptinHER2 crosstalk in breast ...
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    Genre
    Journal Article
    Date
    2008-10-22
    Author
    Fiorio, E
    Mercanti, A
    Terrasi, M
    Micciolo, R
    Remo, A
    Auriemma, A
    Molino, A
    Parolin, V
    Di Stefano, B
    Bonetti, F
    Giordano, A
    Cetto, GL
    Surmacz, E
    Show allShow less
    Subject
    Breast Neoplasms
    Carcinoma, Ductal, Breast
    Cell Line, Tumor
    Female
    Gene Expression Regulation, Neoplastic
    Humans
    Immunohistochemistry
    Leptin
    Obesity
    Postmenopause
    Protein Binding
    Receptor Cross-Talk
    Receptor, ErbB-2
    Receptors, Leptin
    Risk Factors
    Transcriptional Activation
    Show allShow less
    Permanent link to this record
    http://hdl.handle.net/20.500.12613/5599
    
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    DOI
    10.1186/1471-2407-8-305
    Abstract
    Background: 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.
    Citation to related work
    Springer Science and Business Media LLC
    Has part
    BMC Cancer
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    ae974a485f413a2113503eed53cd6c53
    http://dx.doi.org/10.34944/dspace/5581
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