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    請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/13538


    題名: Arginine signaling and cancer metabolism
    作者: Chen, CL;Hsu, SC;Ann, DK;Yen, Y;Kung, HJ
    貢獻者: Institute of Molecular and Genomic Medicine;Institute of Cellular and Systems Medicine
    摘要: Simple Summary In this review, we describe arginine's role as a signaling metabolite, epigenetic regulator and mitochondrial modulator in cancer cells, and summarize recent progress in the application of arginine deprivation as a cancer therapy. Arginine is an amino acid critically involved in multiple cellular processes including the syntheses of nitric oxide and polyamines, and is a direct activator of mTOR, a nutrient-sensing kinase strongly implicated in carcinogenesis. Yet, it is also considered as a non- or semi-essential amino acid, due to normal cells' intrinsic ability to synthesize arginine from citrulline and aspartate via ASS1 (argininosuccinate synthase 1) and ASL (argininosuccinate lyase). As such, arginine can be used as a dietary supplement and its depletion as a therapeutic strategy. Strikingly, in over 70% of tumors, ASS1 transcription is suppressed, rendering the cells addicted to external arginine, forming the basis of arginine-deprivation therapy. In this review, we will discuss arginine as a signaling metabolite, arginine's role in cancer metabolism, arginine as an epigenetic regulator, arginine as an immunomodulator, and arginine as a therapeutic target. We will also provide a comprehensive summary of ADI (arginine deiminase)-based arginine-deprivation preclinical studies and an update of clinical trials for ADI and arginase. The different cell killing mechanisms associated with various cancer types will also be described.
    日期: 2021-07-15
    關聯: Cancers. 2021 Jul 15;13(14):Article number 3541.
    Link to: http://dx.doi.org/10.3390/cancers13143541
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=2072-6694&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000676330700001
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85110488935
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