國家衛生研究院 NHRI:Item 3990099045/11692
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    jsp.display-item.identifier=請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/11692


    题名: c-Myc promotes lymphatic metastasis of pancreatic neuroendocrine tumor through VEGFC upregulation
    作者: Chang, TM;Shan, YS;Chu, PY;Lin, HY;Huang, KW;Hung, WC;Chen, LT;Tsai, HJ
    贡献者: National Institute of Cancer Research
    摘要: Lymphangiogenesis is essential for tumor metastasis via lymphatic system. c-Myc overexpression has been found in many cancers and is involved in tumorigenesis. However, whether c-Myc participates in lymphangiogenesis of pancreatic neuroendocrine tumor (pNET) microenvironment is unclear. We have found that high expression of c-Myc was commonly observed in pNETs previously. In this study, we found that VEGFC expression was increased in human and mouse pNET cell lines with c-Myc overexpression. Mechanistically, c-Myc transcriptionally upregulated VEGFC expression through direct binding to E-box of VEGFC promoter and enhanced VEGFR3 phosphorylation and tube formation of lymphatic endothelial cells. In mouse model, mice bearing pNET cells with c-Myc overexpression had more lymph node metastasis. Combine treatment of mTOR inhibitor, RAD001, with c-Myc inhibitor, 10058-F4, or VEGFC neutralizing chimera protein, VEGFR3/Fc, reduced lymph node metastasis of the mice. Taken together, we demonstrated that c-Myc enhances lymph node metastases via upregulating VEGFC/VEGFR3 axis. Simultaneously targeting mTOR and c-Myc or VEGFC may attenuate c-Myc induced lymphangiogenesis of pNET.
    日期: 2018-12
    關聯: Cancer Science. 2018 Dec;109(Suppl. 2):866.
    Link to: https://doi.org/10.1111/cas.13904
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1347-9032&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000453773604123
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