ArticleBMC biotechnology2025
CDCP1 promotes the malignant phenotypes of nasopharyngeal carcinoma via the Wnt/β-catenin signaling pathway.
Article in BMC biotechnology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Astragaloside IV inhibits nasopharyngeal carcinoma progression by inhibiting SATB2/Wnt/PD-L1 pathway and enhancing the killing activity of T cells.European journal of histochemistry : EJH · 2026Article
- Crosstalk between protein lipidation and ubiquitination in tumor biology.Apoptosis : an international journal on programmed cell death · 2026Review
- A human patient-derived organoid biobank to model tumor heterogeneity and therapeutic vulnerability for oral squamous cell carcinoma.Cell reports. Medicine · 2026Article
- Therapeutic resistance in HPV-positive oropharyngeal squamous cell carcinoma: molecular mechanisms, clinical challenges, and precision strategies.Frontiers in genetics · 2026Review
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Authors and funding
5 authors.
Funding
Abstract
backgroundCUB 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.
methodsThe 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.
resultsCDCP1 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.
conclusionsIn summary, CDCP1 promotes NPC progression via the Wnt/β-catenin pathway, suggesting its potential as a therapeutic target. CLINICAL TRIAL NUMBER: Not applicable.
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