Promotion of metastasis of thyroid cancer cells via NRP-2-mediated induction

doi:10.3892/ol.2016.5153

CNU IR > Pharmacy and Science > Dept. of Food Science & Technology > Periodical Articles > Item 310902800/31029

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

Title:	Promotion of metastasis of thyroid cancer cells via NRP-2-mediated induction
Authors:	Tu, Dom-Gene Chang, Wen-Wei Jan, Ming-Shiou Tu, Chi-Wen Lu, Yin-Che Tai, Chien-Kuo
Contributors:	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
Keywords:	NRP-2 VEGF-C thyroid cancer tumor metastasis lymphangiogenesis
Date:	2016-11
Issue Date:	2018-01-18 11:40:10 (UTC+8)
Publisher:	Spandidos Publ Ltd
Abstract:	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.
Relation:	Oncology Letters, v.12 n.5, pp.4224-4230
Appears in Collections:	[Dept. of Food Science & Technology] Periodical Articles

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