CDCP1通过Wnt/β-连环蛋白信号通路促进鼻咽癌的恶性表型。

CDCP1 promotes the malignant phenotypes of nasopharyngeal carcinoma via the Wnt/β-catenin signaling pathway.

作者信息

Bie Guoliang, Cheng Shuang, Huang Weiping, Yin Zhongpu, Liu Jianzhi

机构信息

Department of Otorhinolaryngology, Fujian Medical University Union Hospital, Fuzhou, Fujian, 350001, China, People's Republic.

Department of Otorhinolaryngology, Liqun Hospital Putuo District, Shanghai, Shanghai, 200333, China, People's Republic.

出版信息

BMC Biotechnol. 2025 Jul 7;25(1):67. doi: 10.1186/s12896-025-01001-4.

DOI:10.1186/s12896-025-01001-4

PMID:40624715

Abstract

BACKGROUND

CUB domain-containing protein 1 (CDCP1), a type I transmembrane glycoprotein, is abundantly expressed in various cancers. However, its role and mechanism in nasopharyngeal carcinoma (NPC) remain ambiguous.

METHODS

The UALCAN and GEPIA databases were analyzed to explore CDCP1 expression and survival prognosis in head and neck squamous cell carcinoma (HNSC) patients. Fifteen pairs of NPC tissues and adjacent normal tissues were collected for CDCP1 expression analysis. CCK-8 assays, flow cytometry, and transwell assays were performed on NPC cell lines (C666-1, 5-8 F, and HONE-1). The impact of GSK-3β inhibitor LiCl on C666-1 cells after CDCP1 knockdown was investigated. A C666-1 xenograft model was established for in vivo validation.

RESULTS

CDCP1 was overexpressed in HNSC patients, and elevated CDCP1 correlated with poor survival. NPC tissues confirmed CDCP1 upregulation compared to normal tissues. CDCP1 knockdown in C666-1 and 5-8 F cells inhibited proliferation, migration, invasion, and promoted apoptosis, while LiCl partially reversed these effects. In vivo, CDCP1 silencing suppressed tumor growth, downregulated PCNA, Wnt3a, β-catenin, and p-GSK-3β, and upregulated cleaved caspase-3 and E-cadherin. CDCP1 overexpression in HONE-1 cells produced opposing effects.

CONCLUSIONS

In summary, CDCP1 promotes NPC progression via the Wnt/β-catenin pathway, suggesting its potential as a therapeutic target.

CLINICAL TRIAL NUMBER

Not applicable.

摘要

背景

含CUB结构域蛋白1（CDCP1）是一种I型跨膜糖蛋白，在多种癌症中大量表达。然而，其在鼻咽癌（NPC）中的作用和机制仍不明确。

方法

分析UALCAN和GEPIA数据库，以探究头颈部鳞状细胞癌（HNSC）患者中CDCP1的表达及生存预后。收集15对NPC组织和癌旁正常组织用于CDCP1表达分析。对NPC细胞系（C666-1、5-8 F和HONE-1）进行CCK-8检测、流式细胞术和Transwell检测。研究CDCP1敲低后GSK-3β抑制剂氯化锂对C666-1细胞的影响。建立C666-1异种移植模型进行体内验证。

结果

HNSC患者中CDCP1过表达，CDCP1升高与不良生存相关。与正常组织相比，NPC组织证实CDCP1上调。C666-1和5-8 F细胞中CDCP1敲低抑制增殖、迁移、侵袭并促进凋亡，而氯化锂部分逆转了这些作用。在体内，CDCP1沉默抑制肿瘤生长，下调PCNA、Wnt3a、β-连环蛋白和p-GSK-3β，并上调裂解的caspase-3和E-钙黏蛋白。HONE-1细胞中CDCP1过表达产生相反的作用。