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    RNAi knockdown of Hop (Hsp70/Hsp90 organising protein) decreases invasion via MMP-2 down regulation.

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    Authors
    Walsh, Naomi
    Larkin, AnneMarie
    Swan, Niall
    Conlon, Kevin
    Dowling, Paul
    McDermott, Ray
    Clynes, Martin
    Affiliation
    National Institute for Cellular Biotechnology, Dublin City University, Glasnevin, Dublin 9, Ireland. Naomi.walsh@dcu.ie
    Issue Date
    2011-07-28
    MeSH
    Adenocarcinoma, Mucinous
    Blotting, Western
    Carcinoma, Pancreatic Ductal
    Cell Adhesion
    Cell Movement
    Down-Regulation
    Gene Expression Regulation, Neoplastic
    HSP70 Heat-Shock Proteins
    HSP90 Heat-Shock Proteins
    Heat-Shock Proteins
    Humans
    Immunoenzyme Techniques
    Immunoprecipitation
    Matrix Metalloproteinase 2
    Molecular Chaperones
    Neoplasm Invasiveness
    Pancreatic Neoplasms
    RNA, Small Interfering
    Tumor Cells, Cultured
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    Citation
    RNAi knockdown of Hop (Hsp70/Hsp90 organising protein) decreases invasion via MMP-2 down regulation. 2011, 306 (2):180-9 Cancer Lett.
    Publisher
    Cancer letters
    Journal
    Cancer letters
    URI
    http://hdl.handle.net/10147/251936
    DOI
    10.1016/j.canlet.2011.03.004
    PubMed ID
    21470770
    Abstract
    We previously identified Hop as over expressed in invasive pancreatic cancer cell lines and malignant tissues of pancreatic cancer patients, suggesting an important role for Hop in the biology of invasive pancreatic cancer. Hop is a co-chaperone protein that binds to both Hsp70/Hsp90. We hypothesised that by targeting Hop, signalling pathways modulating invasion and client protein stabilisation involving Hsp90-dependent complexes may be altered. In this study, we show that Hop knockdown by small interfering (si)RNA reduces the invasion of pancreatic cancer cells, resulting in decreased expression of the downstream target gene, matrix metalloproteinases-2 (MMP-2). Hop in conditioned media co-immunoprecipitates with MMP-2, implicating a possible extracellular function for Hop. Knockdown of Hop expression also reduced expression levels of Hsp90 client proteins, HER2, Bcr-Abl, c-MET and v-Src. Furthermore, Hop is strongly expressed in high grade PanINs compared to lower PanIN grades, displaying differential localisation in invasive ductal pancreatic cancer, indicating that the localisation of Hop is an important factor in pancreatic tumours. Our data suggests that the attenuation of Hop expression inactivates key signal transduction proteins which may decrease the invasiveness of pancreatic cancer cells possibly through the modulation of Hsp90 activity. Therefore, targeting Hop in pancreatic cancer may constitute a viable strategy for targeted cancer therapy.
    Item Type
    Article
    Language
    en
    ISSN
    1872-7980
    ae974a485f413a2113503eed53cd6c53
    10.1016/j.canlet.2011.03.004
    Scopus Count
    Collections
    Tallaght University Hospital

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