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    Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/8699


    Title: Targeting of surface alpha-enolase inhibits the invasiveness of pancreatic cancer cells
    Other Titles: Targeting of surface α-enolase inhibits the invasiveness of pancreatic cancer cells
    Authors: Principe, M;Ceruti, P;Shih, NY;Chattaragada, MS;Rolla, S;Conti, L;Bestagno, M;Zentilin, L;Yang, SH;Migliorini, P;Cappello, P;Burrone, O;Novelli, F
    Contributors: National Institute of Cancer Research
    Abstract: Pancreatic Ductal Adenocarcinoma (PDAC) is a highly aggressive malignancy characterized by rapid progression, invasiveness and resistance to treatment. We have previously demonstrated that most PDAC patients have circulating antibodies against the glycolytic enzyme alpha-enolase (ENO1), which correlates with a better response to therapy and survival. ENO1 is a metabolic enzyme, also expressed on the cell surface where it acts as a plasminogen receptor. ENO1 play a crucial role in cell invasion and metastasis by promoting plasminogen activation into plasmin, a serine-protease involved in extracellular matrix degradation. The aim of this study was to investigate the role of ENO1 in PDAC cell invasion. We observed that ENO1 was expressed on the cell surface of most PDAC cell lines. Mouse anti-human ENO1 monoclonal antibodies inhibited plasminogen-dependent invasion of human PDAC cells, and their metastatic spreading in immunosuppressed mice was inhibited. Notably, a single administration of Adeno-Associated Virus (AAV)-expressing cDNA coding for 72/1 anti-ENO1 mAb reduced the number of lung metastases in immunosuppressed mice injected with PDAC cells. Overall, these data indicate that ENO1 is involved in PDAC cell invasion, and that administration of an anti-ENO1 mAb can be exploited as a novel therapeutic option to increase the survival of metastatic PDAC patients.
    Date: 2015-05
    Relation: Oncotarget. 2015 May;6(13):11098-11113.
    Link to: http://dx.doi.org/10.18632/oncotarget.3572
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000359006400034
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84929611036
    Appears in Collections:[施能耀] 期刊論文

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