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    Please use this identifier to cite or link to this item: http://ir.cnu.edu.tw/handle/310902800/31029


    標題: Promotion of metastasis of thyroid cancer cells via NRP-2-mediated induction
    作者: Tu, Dom-Gene
    Chang, Wen-Wei
    Jan, Ming-Shiou
    Tu, Chi-Wen
    Lu, Yin-Che
    Tai, Chien-Kuo
    貢獻者: Chia Yi Christian Hosp, Dept Nucl Med, Ditmanson Med Fdn
    Chia Nan Univ Pharm & Sci, Dept Food Sci & Technol
    Chang Jung Christian Univ, Coll Hlth Sci
    Chung Shan Med Univ, Sch Biomed Sci, Coll Med Sci & Technol
    Chung Shan Med Univ, Immunol Res Ctr
    Chung Shan Med Univ, Inst Biochem Microbiol & Immunol
    Chia Yi Christian Hosp, Div Allergy Immunol & Rheumatol
    Chia Yi Christian Hosp, Dept Surg, Ditmanson Med Fdn
    Chia Yi Christian Hosp, Dept Hematol Oncol, Ditmanson Med Fdn
    Natl Chung Cheng Univ, Inst Mol Biol, Dept Life Sci
    Natl Chung Cheng Univ, Inst Biomed Sci, Dept Life Sci
    關鍵字: NRP-2
    VEGF-C
    thyroid cancer
    tumor metastasis
    lymphangiogenesis
    日期: 2016-11
    上傳時間: 2018-01-18 11:40:10 (UTC+8)
    出版者: Spandidos Publ Ltd
    摘要: Tumor-node-metastasis is one of the leading causes of morbidity and mortality in thyroid cancer patients. Upregulation of vascular endothelial growth factor-C (VEGF-C) increases the migratory ability of thyroid cancer cells to lymph nodes. Expression of neuropilin-2 (NRP-2), the co-receptor of VEGF-C, has been reported to be correlated with lymph node metastasis in human thyroid cancer. The present study investigated the role of VEGF-C/NRP-2 signaling in the regulation of metastasis of two different types of human thyroid cancer cells. The results indicated that the VEGF-C/NRP-2 axis significantly promoted the metastatic activities of papillary thyroid carcinoma cells through the activation of the mitogen-activated protein kinase (MAPK) kinase (MEK)/extracellular signal-regulated kinase and p38 MAPK signaling cascades. However, neither MEK or p38 MAPK inhibitors produced significant inhibition of the migratory activity and invasiveness regulated by the VEGF-C/NRP-2 axis in follicular thyroid carcinoma cells. Finally, VEGF-C/NRP-2-mediated invasion and migration of thyroid cancer cells required the expression of NRP-2. The present results demonstrate that the promotion of metastasis by VEGF-C is mainly due to the upregulation of NRP-2 in thyroid cancer cells, and this metastatic activity regulated by the VEGF-C/NRP-2 axis provides further insight into the process of tumor metastasis.
    關聯: Oncology Letters, v.12 n.5, pp.4224-4230
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