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    INTU is essential for oncogenic Hh signaling through regulating primary cilia formation in basal cell carcinoma

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    Authors
    Yang, N.
    Leung, E. L.-H.
    Liu, C.
    Li, L.
    Eguether, Thibaut
    Jun Yao, X.-J.
    Jones, E. C.
    Norris, D. A.
    Liu, A.
    Clark, R. A.
    Roop, D. R.
    Pazour, Gregory J.
    Shroyer, K. R.
    Chen, J.
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    UMass Chan Affiliations
    Program in Molecular Medicine
    Document Type
    Journal Article
    Publication Date
    2017-08-31
    Keywords
    Basal cell carcinoma
    Diagnostic markers
    Morphogen signalling
    Transcription
    INTU
    BCC
    cilia
    hedgehog
    skin
    keratinocyte
    Cancer Biology
    Cell Biology
    Developmental Biology
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    Link to Full Text
    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5578876/
    Abstract
    Inturned (INTU), a cilia and planar polarity effector, performs prominent ciliogenic functions during morphogenesis, such as in the skin. INTU is expressed in adult tissues but its role in tissue maintenance is unknown. Here, we report that the expression of the INTU gene is aberrantly elevated in human basal cell carcinoma (BCC), coinciding with increased primary cilia formation and activated hedgehog (Hh) signaling. Disrupting Intu in an oncogenic mutant Smo (SmoM2)-driven BCC mouse model prevented the formation of BCC through suppressing primary cilia formation and Hh signaling, suggesting that Intu performs a permissive role during BCC formation. INTU is essential for intraflagellar transport A complex assembly during ciliogenesis. To further determine whether Intu is directly involved in the activation of Hh signaling downstream of ciliogenesis, we examined the Hh signaling pathway in mouse embryonic fibroblasts, which readily responds to the Hh pathway activation. Depleting Intu blocked Smo agonist-induced Hh pathway activation, whereas the expression of Gli2DeltaN, a constitutively active Gli2, restored Hh pathway activation in Intu-deficient cells, suggesting that INTU functions upstream of Gli2 activation. In contrast, overexpressing Intu did not promote ciliogenesis or Hh signaling. Taken together, data obtained from this study suggest that INTU is indispensable during BCC tumorigenesis and that its aberrant upregulation is likely a prerequisite for primary cilia formation during Hh-dependent tumorigenesis.
    Source

    Oncogene. 2017 Aug 31;36(35):4997-5005. doi: 10.1038/onc.2017.117. Epub 2017 May 1. Link to article on publisher's site

    DOI
    10.1038/onc.2017.117
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/40430
    PubMed ID
    28459465
    Related Resources

    Link to Article in PubMed

    ae974a485f413a2113503eed53cd6c53
    10.1038/onc.2017.117
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