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    標題: Argininosuccinate lyase interacts with cyclin A2 in cytoplasm and modulates growth of liver tumor cells
    作者: Hung, Yu-Hsuan
    Huang, Hau-Lun
    Chen, Wei-Ching
    Yen, Meng-Chi
    Cho, Chien-Yu
    Weng, Tzu-Yang
    Wang, Chih-Yang
    Chen, Yi-Ling
    Chen, Li-Tzong
    Lai, Ming-Derg
    貢獻者: Natl Cheng Kung Univ, Coll Med, Inst Basic Med Sci
    Natl Cheng Kung Univ, Coll Med, Dept Biochem & Mol Biol
    Natl Cheng Kung Univ, Coll Med, Ctr Infect Dis & Signaling Res
    Natl Hlth Res Inst, Natl Inst Canc Res
    Kaohsiung Med Univ,Kaohsiung Med Univ Hosp, Dept Emergency Med
    Chia Nan Univ Pharm & Sci, Dept Senior Citizen Serv Management
    Natl Hlth Res Inst, Natl Inst Canc Res
    關鍵字: argininosuccinate lyase
    liver cancer
    non-enzymatic function
    cyclin A2
    drug resistance
    arginine deiminase
    日期: 2017-02
    上傳時間: 2018-11-30 15:55:00 (UTC+8)
    出版者: Spandidos Publ Ltd
    摘要: Arginine is a critical amino acid in specific cancer types including hepatocellular carcinoma (HCC) and melanoma. Novel molecular mechanisms and therapeutic targets in arginine metabolism-mediated cancer formation await further identification. Our laboratory has previously demonstrated that arginine metabolic enzyme argininosuccinate lyase (ASL) promoted HCC formation in part via maintenance of cyclin A2 protein expression and arginine production for channeling to nitric oxide synthase. In this study, we investigated the mechanism by which ASL regulates cyclin A2 expression. We found that ASL interacted with cyclin A2 in HCC cells and the localization of their interaction was in the cytoplasm. Mutation of essential residues for enzymatic activity of ASL did not affect the binding of ASL to cyclin A2. Moreover, the mutant ASL retained the ability to restore the decreased tumorigenicity caused by ASL shRNA. Furthermore, overexpression of ASL conferred resistance to arginine deprivation therapy. Finally, the important pathways and potential therapeutic targets in ASL-regulated HCC were identified by bioinformatics analyses with Metacore database and Connectivity Map database. Our analyses suggested that bisoprolol, celecoxib, and ipratropium bromide, are potential therapeutics for ASL-regulated HCC formation. Thus, ASL interacts with cyclin A2 in cytoplasm, and may promote HCC formation through this non-enzymatic function. Overexpression of ASL may be a contributing factor in drug resistance for arginine deprivation therapy.
    關聯: Oncology Reports, v.37, n.2, pp.969-978
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