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    Please use this identifier to cite or link to this item: https://ir.csmu.edu.tw:8080/ir/handle/310902500/15698


    Title: Isoliquiritigenin as a cause of DNA damage and inhibitor of ataxia-telangiectasia mutated expression leading to G2/M phase arrest and apoptosis in oral squamous cell carcinoma.
    Authors: SM, Hsia;CC, Yu;YH, Shih;Yuanchien, Chen M;TH, Wang;YT, Huang;TM, Shieh
    Contributors: 中山醫大口腔科學研究所
    http://dx.doi.org/10.1002/hed.24001
    Keywords: DNA damage;apoptosis;ataxia telangiectasia mutated (ATM);isoliquiritigenin;oral squamous cell carcinoma
    Date: 2015-06-16
    Issue Date: 2016-08-09T08:30:02Z (UTC)
    ISSN: 1043-3074
    Abstract: BACKGROUND:
    Isoliquiritigenin (ISL), a natural compound extracted from licorice, has chemopreventive and antitumor activities. The purpose of this study was to investigate the anticancer effect of ISL on human oral squamous cell carcinoma (OSCC).
    METHODS:
    The anti-OSCC effects of ISL were evaluated using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide test, flow cytometry, reverse transcription-polymerase chain reaction, Western blotting, promoter activity, terminal deoxynucleotidyl transferase dUTP nick-end labeling assay, malignant phenotype analysis, microRNA, and xenografting.
    RESULTS:
    ISL induced OSCC cell cycle G2/M phase arrest, apoptosis, and DNA damage. However, the DNA repair-associated ataxia telangiectasia mutated (ATM) and phospho-ATM were downregulated, ATM mRNA remained unchanged, and the downstream signals were inhibited. ATM recovered when the caspase activity was blocked by Z-DVED-FMK. A low dose of ISL inhibited OSCC malignancy in vitro and reduced the tumor size in vivo.
    CONCLUSION:
    ATM was cleaved by ISL-activated caspase, thus inhibiting DNA repair in OSCC cells. Therefore, ISL is a promising chemopreventive agent against oral cancer. © 2015 Wiley Periodicals, Inc. Head Neck 38: E360-E371, 2016.
    URI: https://ir.csmu.edu.tw:8080/ir/handle/310902500/15698
    Relation: Head Neck. 2016 Apr;38 Suppl 1:E360-71.
    Appears in Collections:[牙醫學系暨碩士班] 期刊論文

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