Logo for the University of Illinois at Chicago
    • Login
    View Item 
    •   INDIGO Home
    • UIC Cancer Center
    • Publications - Cancer Center
    • View Item
    •   INDIGO Home
    • UIC Cancer Center
    • Publications - Cancer Center
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Decorin-mediated inhibition of colorectal cancer growth and migration is associated with E-Cadherin in vitro and in mice

    Thumbnail
    View/Open
    Main Article (1.009Mb)
    Date
    2012-02
    Author
    Bi, Xiuli
    Qian, Zhibin
    Yang, George R.
    Gou, Yuan
    Guzman, Grace
    Balla, Andre
    Iozzo, Renato V.
    Yang, Wancai
    Pohl, Nicole M.
    Publisher
    Oxford University Press
    Metadata
    Show full item record
    Abstract
    Previous studies have shown that decorin expression is significantly reduced in colorectal cancer tissues and cancer cells, and genetic deletion of the decorin gene is sufficient to cause intestinal tumor formation in mice, resulting from a downregulation of p21, p27kip1 and E-Cadherin and an upregulation of β-catenin signaling (Bi et al. Carcinogenesis, 2008). However, the regulation of E-Cadherin by decorin and its implication in cancer formation and metastasis is largely unknown. Using a decorin knockout mouse model (Dcn-/- mice) and manipulated expression of decorin in human colorectal cancer cells we found that E-Cadherin, a protein that regulates cell-cell adhesion, epithelial-mesenchymal transition and metastasis, was almost completely lost in Dcn-/- mouse intestine, and loss of decorin and E-Cadherin accelerated colon cancer cell growth and invasion in Dcn- /- mice. However, increasing decorin expression in colorectal cancer cells attenuated cancer cell malignancy, including inhibition of cancer cell proliferation, promotion of apoptosis, and importantly, attenuation of cancer cell migration. All these changes were linked to the regulation of E-Cadherin by decorin. Moreover, overexpression of decorin upregulated E-Cadherin through increasing of ECadherin protein stability as E-Cadherin mRNA and promoter activity were not affected. Co-immunoprecipitation assay showed a physical binding between decorin and E-Cadherin proteins. Taken together, our results provide direct evidence that decorin-mediated inhibition of colorectal cancer growth and migration is through the interaction with and stabilization of E-Cadherin.
    Type
    Article
    Date available in INDIGO
    2013-12-06T19:01:36Z
    URI
    http://hdl.handle.net/10027/10422
    Collections
    • Publications - Cancer Center

    DSpace software copyright © 2002-2015  DuraSpace
    Contact Us | Send Feedback | Privacy Statement
    Theme by 
    Atmire NV

    Browse

    All of INDIGOCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsThis CollectionBy Issue DateAuthorsTitlesSubjects

    My Account

    LoginRegister

    Statistics

    View Usage Statistics

    DSpace software copyright © 2002-2015  DuraSpace
    Contact Us | Send Feedback | Privacy Statement
    Theme by 
    Atmire NV