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  • Sox2 modulates motility and enhances progression of colorectal cancer via the Rho-ROCK signaling pathway

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    Author
    Zheng, Junheng
    Xu, Lixiao
    Pan, Yubin
    Yu, Shuyi
    Wang, Hongbo
    Kennedy, Derek
    Zhang, Yan
    Year published
    2017
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    Abstract
    Sox2 (Sry-box2) is essential for a variety of stem cells and is also expressed in colorectal cancer (CRC). However, the underlying mechanism by which Sox2 enhances CRC progression remains unclear. In the present study, we show that elevated Sox2 expression is significantly correlated with poor clinical prognosis. CRC is phenotypically heterogeneous, and harbors several subtypes of cancer cells. Elevated Sox2 expression was always detected in rounded-shape cells, which co-located to poorly differentiated regions, the invasive frontier and metastatic lesions. Knockdown of Sox2 in CRC cells not only decreased the number of round-shaped cells, but also suppressed cell migration, invasion as well as attenuated colony forming capacity and tumorigenicity. By contrast, overexpression of Sox2 in CRC cells was associated with up-regulation of multidrug resistance genes and accelerated CRC progression. Moreover, Sox2 conferred activation of Rho-ROCK signaling, whereas inhibition of ROCK signaling decreased cell migration, invasion, colony formation and self-renewal of CRC. Our results reveal that CRC is phenotypically and functionally heterogeneous. Elevated Sox2 expression activates the Rho-ROCK pathway, which in turn changes cell morphology and promotes cell migration and progression.
    Journal Title
    Oncotarget
    Volume
    8
    Issue
    58
    DOI
    https://doi.org/10.18632/oncotarget.21709
    Copyright Statement
    © Zheng et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
    Subject
    Oncology and Carcinogenesis not elsewhere classified
    Publication URI
    http://hdl.handle.net/10072/372003
    Collection
    • Journal articles

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