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    Noncoding mutations target cis-regulatory elements of the FOXA1 plexus in prostate cancer

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    Authors
    Zhou, S
    Hawley, JR
    Soares, F
    Grillo, G
    Teng, M
    Madani, Tonekaboni SA
    Hua, JT
    Kron, KJ
    Mazrooei, P
    Ahmed, M
    Arlidge, C
    Yun, HY
    Livingstone, J
    Huang, V
    Yamaguchi, TN
    Espiritu, SMG
    Zhu, Y
    Severson, TM
    Murison, A
    Cameron, S
    Zwart, W
    Van der Kwast, T
    Pugh, TJ
    Fraser, M
    Boutros, PC
    Bristow, Robert G
    He, HH
    Lupien, M
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    Affiliation
    Princess Margaret Cancer Centre, University Health Network, Toronto, ON, Canada
    Issue Date
    2020
    
    Metadata
    Show full item record
    Abstract
    Prostate cancer is the second most commonly diagnosed malignancy among men worldwide. Recurrently mutated in primary and metastatic prostate tumors, FOXA1 encodes a pioneer transcription factor involved in disease onset and progression through both androgen receptor-dependent and androgen receptor-independent mechanisms. Despite its oncogenic properties however, the regulation of FOXA1 expression remains unknown. Here, we identify a set of six cis-regulatory elements in the FOXA1 regulatory plexus harboring somatic single-nucleotide variants in primary prostate tumors. We find that deletion and repression of these cis-regulatory elements significantly decreases FOXA1 expression and prostate cancer cell growth. Six of the ten single-nucleotide variants mapping to FOXA1 regulatory plexus significantly alter the transactivation potential of cis-regulatory elements by modulating the binding of transcription factors. Collectively, our results identify cis-regulatory elements within the FOXA1 plexus mutated in primary prostate tumors as potential targets for therapeutic intervention.
    Citation
    Zhou S, Hawley JR, Soares F, Grillo G, Teng M, Madani Tonekaboni SA, et al. Noncoding mutations target cis-regulatory elements of the FOXA1 plexus in prostate cancer. Nat Commun. 2020;11(1):441.
    Journal
    Nature Communications
    URI
    http://hdl.handle.net/10541/622765
    DOI
    10.1038/s41467-020-14318-9
    PubMed ID
    31974375
    Additional Links
    https://dx.doi.org/10.1038/s41467-020-14318-9
    Type
    Article
    Language
    en
    ae974a485f413a2113503eed53cd6c53
    10.1038/s41467-020-14318-9
    Scopus Count
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    All Paterson Institute for Cancer Research

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