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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/7791


    Title: Leukocyte cell-derived chemotaxin 2 antagonizes MET receptor activation to suppress hepatocellular carcinoma vascular invasion by protein tyrosine phosphatase 1B recruitment
    Authors: Chen, CK;Yang, CY;Hua, KT;Ho, MC;Johansson, G;Jeng, YM;Chen, CN;Chen, MW;Lee, WJ;Su, JL;Lai, TC;Chou, CC;Ho, BC;Chang, CF;Lee, PH;Chang, KJ;Hsiao, M;Lin, MT;Kuo, ML
    Contributors: National Institute of Cancer Research
    Abstract: Leukocyte cell-derived chemotoxin 2 (LECT2) has been shown to act as a tumor suppressor in hepatocellular carcinoma (HCC). However, the underlying mechanism has not yet been completely defined. Here, we employ a LECT2-affinity column plus liquid chromatography coupled with tandem mass spectrometry to identify LECT2-binding proteins and found that MET receptor strongly interacted with LECT2 protein. Despite the presence of hepatocyte growth factor, the LECT2 binding causes an antagonistic effect to MET receptor activation through recruitment of protein tyrosine phosphatase 1B. The antagonistic effect of LECT2 on MET activation also mainly contributes to the blockage of vascular invasion and metastasis of HCC. Furthermore, serial deletions and mutations of LECT2 showing that the HxGxD motif is primarily responsible for MET receptor binding and its antagonistic effects. Our findings reveal a novel, specific inhibitory function of LECT2 in HCC by the direct binding and inactivation of MET, opening a potential avenue for treating MET-related cancer.
    Date: 2014-03
    Relation: Hepatology. 2014 Mar;59(3):974-985.
    Link to: http://dx.doi.org/10.1002/hep.26738
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0270-9139&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000331787500027
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84896701555
    Appears in Collections:[蘇振良] 期刊論文

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