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    Modeling ductal carcinoma in situ: a HER2-Notch3 collaboration enables luminal filling.

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    Authors
    Pradeep, C-R
    Köstler, W J
    Lauriola, M
    Granit, R Z
    Zhang, F
    Jacob-Hirsch, J
    Rechavi, G
    Nair, H B
    Hennessy, B T
    Gonzalez-Angulo, A M
    Tekmal, R R
    Ben-Porath, I
    Mills, G B
    Domany, E
    Yarden, Y
    Show allShow less
    Affiliation
    Department of Biological Regulation, The Weizmann Institute of Science, Rehovot, Israel.
    Issue Date
    2012-02-16
    MeSH
    Animals
    Breast Neoplasms
    Carcinoma, Intraductal, Noninfiltrating
    Cell Line
    Cell Proliferation
    Epidermal Growth Factor
    Epithelial Cells
    Female
    Gene Expression Profiling
    Green Fluorescent Proteins
    HEK293 Cells
    Humans
    Immunoblotting
    Mammary Glands, Human
    Mice
    Mice, Transgenic
    Microscopy, Confocal
    Models, Biological
    Oligonucleotide Array Sequence Analysis
    RNA Interference
    Receptor, erbB-2
    Receptors, Notch
    Reverse Transcriptase Polymerase Chain Reaction
    Signal Transduction
    Transfection
    Show allShow less
    
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    Citation
    Modeling ductal carcinoma in situ: a HER2-Notch3 collaboration enables luminal filling. 2012, 31 (7):907-17 Oncogene
    Journal
    Oncogene
    URI
    http://hdl.handle.net/10147/230452
    DOI
    10.1038/onc.2011.279
    PubMed ID
    21743488
    Abstract
    A large fraction of ductal carcinoma in situ (DCIS), a non-invasive precursor lesion of invasive breast cancer, overexpresses the HER2/neu oncogene. The ducts of DCIS are abnormally filled with cells that evade apoptosis, but the underlying mechanisms remain incompletely understood. We overexpressed HER2 in mammary epithelial cells and observed growth factor-independent proliferation. When grown in extracellular matrix as three-dimensional spheroids, control cells developed a hollow lumen, but HER2-overexpressing cells populated the lumen by evading apoptosis. We demonstrate that HER2 overexpression in this cellular model of DCIS drives transcriptional upregulation of multiple components of the Notch survival pathway. Importantly, luminal filling required upregulation of a signaling pathway comprising Notch3, its cleaved intracellular domain and the transcriptional regulator HES1, resulting in elevated levels of c-MYC and cyclin D1. In line with HER2-Notch3 collaboration, drugs intercepting either arm reverted the DCIS-like phenotype. In addition, we report upregulation of Notch3 in hyperplastic lesions of HER2 transgenic animals, as well as an association between HER2 levels and expression levels of components of the Notch pathway in tumor specimens of breast cancer patients. Therefore, it is conceivable that the integration of the Notch and HER2 signaling pathways contributes to the pathophysiology of DCIS.
    Item Type
    Article
    Language
    en
    ISSN
    1476-5594
    ae974a485f413a2113503eed53cd6c53
    10.1038/onc.2011.279
    Scopus Count
    Collections
    Beaumont Hospital

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