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    Extracellular matrix (ECM) activates β-catenin signaling in uterine fibroids

    Access Status
    Fulltext not available
    Authors
    Ko, Y.
    Jamaluddin, M.
    Adebayo, M.
    Bajwa, P.
    Scott, R.
    Dharmarajan, Arunasalam
    Nahar, P.
    Tanwar, P.
    Date
    2018
    Type
    Journal Article
    
    Metadata
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    Citation
    Ko, Y. and Jamaluddin, M. and Adebayo, M. and Bajwa, P. and Scott, R. and Dharmarajan, A. and Nahar, P. et al. 2018. Extracellular matrix (ECM) activates β-catenin signaling in uterine fibroids. Reproduction. 155 (1): pp. 61-71.
    Source Title
    Reproduction
    DOI
    10.1530/REP-17-0339
    ISSN
    1470-1626
    School
    School of Pharmacy and Biomedical Sciences
    URI
    http://hdl.handle.net/20.500.11937/68225
    Collection
    • Curtin Research Publications
    Abstract

    Recent studies showed that genetic aberrations in the MED12 gene, probably through the canonical WNT/β-catenin pathway, lead to the pathogenesis of uterine fibroids. However, a comprehensive analysis of the WNT pathway in MED12-mutated and MED12-wild-type fibroids has not been performed. The objective of this study was to determine the status of the WNT pathway in human fibroids. We performed Sanger sequencing to define the MED12 mutational status of fibroids and normal myometrium samples. qPCR arrays were carried out to determine the status of the WNT signaling pathway in MED12-mutated and MED12-wild-type fibroids. Liquid chromatography–mass spectrometry (LC–MS), Western blotting and immunohistochemistry were used to monitor the expression of β-catenin. We showed that β-catenin expression was increased in fibroids compared to the adjacent myometrium samples. However, β-catenin expression showed no correlation with MED12 mutation status. Of all the WNT signaling components, WNT inhibitors showed the greatest differences in expression between fibroids and controls. WIF1, a WNT inhibitor, was identified as the most significantly upregulated gene in fibroids. We cultured primary fibroid cells on hydrogels of known stiffness to decipher the influence of biomechanical cues on β-catenin expression and revealed increased levels of β-catenin when cells were cultured on a stiffer surface. In conclusion, our data showed that β-catenin expression in fibroids occurs independently of MED12 mutations. Biomechanical changes upregulate β-catenin expression in fibroids, providing an attractive avenue for developing new treatments for this disease.

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