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    Multiplexed Quantum Dot Labeling of Activated c-Met Signaling in Castration-Resistant Human Prostate Cancer

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    Date
    2011-12-21
    Author
    Hu, Peizhen
    Chu, Gina C.-Y.
    Zhu, Guodong
    Yang, Hua
    Luthringer, Daniel
    Prins, Gail
    Habib, Fouad
    Wang, Yuzhuo
    Wang, Ruoxiang
    Chung, Leland W. K.
    Zhau, Haiyen E.
    Publisher
    Public Library of Science
    Metadata
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    Abstract
    The potential application of multiplexed quantum dot labeling (MQDL) for cancer detection and prognosis and monitoring therapeutic responses has attracted the interests of bioengineers, pathologists and cancer biologists. Many published studies claim that MQDL is effective for cancer biomarker detection and useful in cancer diagnosis and prognosis, these studies have not been standardized against quantitative biochemical and molecular determinations. In the present study, we used a molecularly characterized human prostate cancer cell model exhibiting activated c-Met signaling with epithelial to mesenchymal transition (EMT) and lethal metastatic progression to bone and soft tissues as the gold standard, and compared the c-Met cell signaling network in this model, in clinical human prostate cancer tissue specimens and in a castration-resistant human prostate cancer xenograft model. We observed c-Met signaling network activation, manifested by increased phosphorylated c-Met in all three. The downstream survival signaling network was mediated by NF-kB and Mcl-1 and EMT was driven by receptor activator of NF-kB ligand (RANKL), at the single cell level in clinical prostate cancer specimens and the xenograft model. Results were confirmed by real-time RT-PCR and western blots in a human prostate cancer cell model. MQDL is a powerful tool for assessing biomarker expression and it offers molecular insights into cancer progression at both the cell and tissue level with high degree of sensitivity.
    Type
    Article
    Date available in INDIGO
    2012-08-21T02:44:23Z
    URI
    http://hdl.handle.net/10027/8602
    Collections
    • Publications - Physiology and Biophysics

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