國家衛生研究院 NHRI:Item 3990099045/9971
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    題名: KDM4A coactivates E2F1 to regulate the PDK-dependent metabolic switch between mitochondrial oxidation and glycolysis
    作者: Wang, LY;Hung, CL;Chen, YR;Yang, JC;Wang, J;Campbell, M;Izumiya, Y;Chen, HW;Wang, WC;Ann, DK;Kung, HJ
    貢獻者: Institute of Molecular and Genomic Medicine
    摘要: The histone lysine demethylase KDM4A/JMJD2A has been implicated in prostate carcinogenesis through its role in transcriptional regulation. Here, we describe KDM4A as a E2F1 coactivator and demonstrate a functional role for the E2F1-KDM4A complex in the control of tumor metabolism. KDM4A associates with E2F1 on target gene promoters and enhances E2F1 chromatin binding and transcriptional activity, thereby modulating the transcriptional profile essential for cancer cell proliferation and survival. The pyruvate dehydrogenase kinases (PDKs) PDK1 and PDK3 are direct targets of KDM4A and E2F1 and modulate the switch between glycolytic metabolism and mitochondrial oxidation. Downregulation of KDM4A leads to elevated activity of pyruvate dehydrogenase and mitochondrial oxidation, resulting in excessive accumulation of reactive oxygen species. The altered metabolic phenotypes can be partially rescued by ectopic expression of PDK1 and PDK3, indicating a KDM4A-dependent tumor metabolic regulation via PDK. Our results suggest that KDM4A is a key regulator of tumor metabolism and a potential therapeutic target for prostate cancer.
    日期: 2016-09-13
    關聯: Cell Reports. 2016 Sep 13;16(11):3016-3027.
    Link to: http://dx.doi.org/10.1016/j.celrep.2016.08.018
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=2211-1247&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000383882300021
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84991384391
    顯示於類別:[龔行健] 期刊論文

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