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    國家衛生研究院 NHRI > 癌症研究所 > 其他 > 期刊論文 >  Item 3990099045/13138
    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/13138


    Title: Roles of lysyl oxidase family members in the tumor microenvironment and progression of liver cancer
    Authors: Lin, HY;Li, CJ;Yang, YL;Huang, YH;Hsiau, YT;Chu, PY
    Contributors: National Institute of Cancer Research
    Abstract: The lysyl oxidase (LOX) family members are secreted copper-dependent amine oxidases, comprised of five paralogues: LOX and LOX-like l-4 (LOXL1-4), which are characterized by catalytic activity contributing to the remodeling of the cross-linking of the structural extracellular matrix (ECM). ECM remodeling plays a key role in the angiogenesis surrounding tumors, whereby a corrupt tumor microenvironment (TME) takes shape. Primary liver cancer includes hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), ranked as the seventh most common cancer globally, with limited therapeutic options for advanced stages. In recent years, a growing body of evidence has revealed the key roles of LOX family members in the pathogenesis of liver cancer and the shaping of TME, indicating their notable potential as therapeutic targets. We herein review the clinical value and novel biological roles of LOX family members in tumor progression and the TME of liver cancers. In addition, we highlight recent insights into their mechanisms and their potential involvement in the development of target therapy for liver cancer.
    Date: 2020-12-21
    Relation: International Journal of Molecular Sciences. 2020 Dec 21;21(24):Article number 9751.
    Link to: http://dx.doi.org/10.3390/ijms21249751
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1422-0067&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000602761200001
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85098330510
    Appears in Collections:[其他] 期刊論文

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