Abstract
Nasopharyngeal carcinoma (NPC) has the highest metastatic rate among head and neck cancers, with its underlying mechanism not yet fully unveiled. High- versus low-metastasis, NPC cell lines have been established. The footpad-popliteal lymph node metastasis model and other in vivo models have been stably used to study NPC metastasis. The histological appearance and the expression of epithelial-to-mesenchymal transition (EMT) markers might be helpful in selecting high-risk NPC patients for developing post-treatment metastasis. Tested EMT markers and their protein expression levels that correlate with patient disease-free survival in large patient cohorts include E-cadherin, N-cadherin, CD44, Twist, Snail, and Cyclin D1. Epstein-Barr virus (EBV) infection can trigger NPC metastasis from multiple angles via multiple signaling pathways. High endothelial venules are commonly seen in NPC tissues, with their role in NPC metastasis requiring clarification. The molecules that promote and inhibit NPC metastasis are introduced, with a focus on cytokines SPINK6, serglycin, interleukin 8 (IL8), Wnt family member 5A (WNT5A), and chemokine C-C motif ligand 2 (CCL2). Two videos showing NPC cells with and without SPINK6 knocked down are presented. Future directions for studying NPC metastasis are also discussed.
Highlights
The nasopharynx is covered with squamous epithelium, ciliated columnar epithelium, and some transitional regions of these two epithelial types [1]
Primary Nasopharyngeal carcinoma (NPC) is sensitive to radiotherapy and chemotherapy, 15–18.5% of new NPC patients without distant metastasis will eventually fail from locoregional treatment caused by post-treatment metastasis of the tumor cells [11,12,13]
Our group revealed that SPINK6 is the ligand of epidermal growth factor receptor (EGFR) in NPC cells which induces the dimerization of EGFR and results in activating downstream AKT signaling for metastasis, and this function of SPINK6 is independent of its serine protease-inhibitory activity [37]
Summary
Ling-Ling Guo1,a, Hai-Yun Wang2,3,a, Li-Sheng Zheng, Ming-Dian Wang, Yun Cao, Yang Li5,6, Zhi-Jie Liu, Li-Xia Peng, Bi-Jun Huang, Jian-Yong Shao, and Chao-Nan Qian1,7,*. High- versus low-metastasis, NPC cell lines have been established. The footpad-popliteal lymph node metastasis model and other in vivo models have been stably used to study NPC metastasis. The histological appearance and the expression of epithelial-to-mesenchymal transition (EMT) markers might be helpful in selecting high-risk NPC patients for developing post-treatment metastasis. Epstein-Barr virus (EBV) infection can trigger NPC metastasis from multiple angles via multiple signaling pathways. High endothelial venules are commonly seen in NPC tissues, with their role in NPC metastasis requiring clarification. The molecules that promote and inhibit NPC metastasis are introduced, with a focus on cytokines SPINK6, serglycin, interleukin 8 (IL8), Wnt family member 5A (WNT5A), and chemokine C-C motif ligand 2 (CCL2). Two videos showing NPC cells with and without SPINK6 knocked down are presented. Future directions for studying NPC metastasis are discussed
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