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    Histone demethylase JMJD1A promotes expression of DNA repair factors and radio-resistance of prostate cancer cells

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    Author
    Fan, L.
    Xu, S.
    Zhang, F.
    Cui, X.
    Clark, D.J.
    Yang, A.
    Hussain, A.
    Rassool, F.
    Qi, J.
    Date
    2020
    Journal
    Cell Death and Disease
    Publisher
    Springer Nature
    Type
    Article
    
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    See at
    https://doi.org/10.1038/s41419-020-2405-4
    Abstract
    The DNA damage response (DDR) pathway is a promising target for anticancer therapies. The androgen receptor and myeloblastosis transcription factors have been reported to regulate expression of an overlapping set of DDR genes in prostate cancer cells. Here, we found that histone demethylase JMJD1A regulates expression of a different set of DDR genes largely through c-Myc. Inhibition of JMJD1A delayed the resolution of γ-H2AX foci, reduced the formation of foci containing ubiquitin, 53BP1, BRCA1 or Rad51, and inhibited the reporter activity of double-strand break (DSB) repair. Mechanistically, JMJD1A regulated expression of DDR genes by increasing not only the level but also the chromatin recruitment of c-Myc through H3K9 demethylation. Further, we found that ubiquitin ligase HUWE1 induced the K27-/K29-linked noncanonical ubiquitination of JMJD1A at lysine-918. Ablation of the JMJD1A noncanonical ubiquitination lowered DDR gene expression, impaired DSB repair, and sensitized response of prostate cells to irradiation, topoisomerase inhibitors or PARP inhibitors. Thus, development of agents that target JMJD1A or its noncanonical ubiquitination may sensitize the response of prostate cancer to radiotherapy and possibly also genotoxic therapy. Copyright 2020, The Author(s).
    Sponsors
    This study is supported by NCI grant R01CA207118 and a V Scholar award (to J.Q.). Part of A.H.'s time was supported by a Merit Review Award (I01 BX000545), Medical Research Service, Department of Veterans Affairs.
    Keyword
    Prostrate--Cancer
    Transcription Factors
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85082790577&doi=10.1038%2fs41419-020-2405-4&partnerID=40&md5=bede8e0aaf6c59de4d012601769693eb; http://hdl.handle.net/10713/12542
    ae974a485f413a2113503eed53cd6c53
    10.1038/s41419-020-2405-4
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