远处转移是治疗鼻咽癌（NPC）的主要障碍。肿瘤远程转移是一个复杂的过程，涉及多个癌基因、抑癌基因和与转移有关的基因的共同参与。目前缺乏足够准确的预后基因以评估转移风险。我们旨在寻找更精确的NPC转移生物标志物。我们通过加权基因共表达网络分析、差异表达基因分析、单变量和多变量逐步Cox回归以及Kaplan-Meier（K-M）生存分析，在从10个NPC样品和公共数据库获取的RNA测序数据上进行了研究，确定了与NPC转移相关的关键基因。我们进行创伤愈合实验证实了我们的生物信息学结论。我们进行了转形试验、跨膜试验和免疫组化实验来验证我们的生物信息学结论。我们进行了免疫印迹实验来评估和量化已鉴定的转移相关基因对NPC的上皮间质转化（EMT）的影响。结合我们自己的RNA测序数据和公共数据，我们确定了胰蛋白酶类似蛋白（CPVL）作为NPC的一种抑癌基因。通路富集分析表明，与CPVL相关的基因参与了EMT过程。CPVL表达低的NPC具有高肿瘤纯度和低免疫细胞水平。实验结果显示，CPVL蛋白主要在细胞质和膜中表达，并且在没有远程转移的NPC组织中表达水平更高。CPVL抑制了NPC细胞的迁移和侵袭能力。CPVL的过表达上调了E-cadherin和ZO-1的表达，而下调了vimentin的表达，说明CPVL通过抑制EMT来抑制肿瘤转移。CPVL抑制了NPC细胞的迁移和侵袭，通过上调上皮标记物和抑制间质标记物的表达与肿瘤转移抑制有关，并且可能成为NPC转移风险评估的预后生物标志物。© 2023. 作者, 专属于 Springer-Verlag GmbH Germany, 是 Springer Nature 的一部分。

Distant metastasis is the main obstacle to treating nasopharyngeal carcinoma (NPC). Tumor distance metastasis is a complex process involving the jointly participation of multiple oncogenes, tumor suppressor genes, and metastasis-associated genes. Enough accurate prognostic genes for evaluating metastasis risk are lacking. We aimed to identify more precise biomarkers for NPC metastasis.We performed weighted gene co-expression network analysis, differentially expressed gene analysis, univariate and multivariate stepwise Cox regression, and Kaplan-Meier (K-M) survival analyses, on data obtained from RNA sequencing of 10 NPC samples and the public database, to identify key genes correlated with NPC metastasis. Wound healing assays, transwell assays, and immunohistochemistry were conducted to validate our bioinformatic conclusions. Western blotting was performed to evaluate and quantify the effect of identified EMT genes on epithelial-mesenchymal transition (EMT) of NPC.Combined our own RNA sequencing data and public data, we determined carboxypeptidase vitellogenic-like protein (CPVL) as a tumor suppressor for NPC. Pathway enrichment analyses indicated that genes associated with CPVL are involved in EMT. NPC with low CPVL expression had high tumor purity and low levels of immune cells. Experimental results showed that CPVL protein predominantly expressed in cytoplasmic and membranous and it exhibited higher expression levels in NPC tissues without distant metastasis than those with distant metastasis. CPVL inhibits the migration and invasive capability of NPC cells. Overexpression of CPVL upregulates E-cadherin and ZO-1, whereas it downregulates vimentin, suggesting that CPVL suppresses tumor metastasis by inhibiting EMT.CPVL inhibits migration and invasion of NPC cells and is associated with tumor metastasis suppression through upregulating epithelial marker and inhibiting mesenchymal marker expression and could be a prognostic biomarker for metastasis risk evaluation in NPC.© 2023. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.