Vis Cancer Med
Volume 2, 2021
|Number of page(s)||13|
|Published online||11 August 2021|
Metastasis of nasopharyngeal carcinoma: What we know and do not know
State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Sun Yat-Sen University Cancer Center, Guangzhou 510060, PR China
2 Guangzhou Institute of Pediatrics, Guangzhou Women and Children’s Medical Center, Guangzhou 510623, PR China
3 Department of Molecular Diagnostics, Sun Yat-Sen University Cancer Center, Guangzhou 510060, PR China.
4 Department of Pathology, Sun Yat-Sen University Cancer Center, Guangzhou 510060, PR China
5 Department of Pathology, the First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, PR China
6 Department of Pathology, Guangzhou Concord Cancer Center, Guangzhou 510555, PR China
7 Department of Radiation Oncology, Guangzhou Concord Cancer Center, Guangzhou 510555, PR China
* Corresponding author: firstname.lastname@example.org
Accepted: 6 July 2021
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.
Key words: Nasopharyngeal carcinoma / Metastasis promoter / Metastasis inhibitor / High endothelial venule / Pre-metastatic niche / Epithelial-to-mesenchymal transition / EGFR / SPINK6 / Video / Epstein-Barr virus / Time-lapse photography
© The Authors, published by EDP Sciences, 2021
This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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