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    Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/23451


    Title: A novel melatonin-regulated lncRNA suppresses TPA-induced oral cancer cell motility through replenishing PRUNE2 expression
    Authors: Su, SC;Yeh, CM;Lin, CW;Hsieh, YH;Chuang, CY;Tang, CH;Lee, YC;Yang, SF
    Keywords: lncRNA;melatonin;metastasis;oral cancer
    Date: 2021
    Issue Date: 2022-08-05T09:37:30Z (UTC)
    Publisher: WILEY
    ISSN: 0742-3098
    Abstract: The inhibitory effect of melatonin on cancer cell dissemination is well established, yet the functional involvement of lncRNAs in melatonin signaling remains poorly understood. In this study, we identified a melatonin-attenuated lncRNA acting as a potential melatonin-regulated oral cancer stimulator (MROS-1). Downregulation of MROS-1 by melatonin suppressed TPA-induced oral cancer migration through replenishing the protein expression of prune homolog 2 (PRUNE2), which functioned as a tumor suppressor in oral cancer. Melatonin-mediated MROS-1/PRUNE2 expression and cell motility in oral cancer were regulated largely through the activation of JAK-STAT pathway. In addition, MROS-1, preferentially localized in the nuclei, promoted oral cancer migration in an epigenetic mechanism in which it modulates PRUNE2 expression by interacting with a member of the DNA methylation machinery, DNA methyltransferase 3A (DNMT3A). Higher methylation levels of PRUNE2 promoter were associated with nodal metastases and inversely correlated with PRUNE2 expression in head and neck cancer. Collectively, these findings suggest that MROS-1, serving as a functional mediator of melatonin signaling, could predispose patients with oral cancer to metastasize and may be implicated as a potential target for antimetastatic therapies.
    URI: http://dx.doi.org/10.1111/jpi.12760
    https://www.webofscience.com/wos/woscc/full-record/WOS:000688565500001
    https://ir.csmu.edu.tw:8080/handle/310902500/23451
    Relation: JOURNAL OF PINEAL RESEARCH ,2021,v71,issue 3
    Appears in Collections:[中山醫學大學研究成果] 期刊論文

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