ArticleJournal of experimental & clinical cancer research : CR2025
PXDN regulated by WTAP/YTHDF1-mediated m
Article in Journal of experimental & clinical cancer research : CR, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Deep learning-driven discovery of anti-metastatic phytochemicals targeting MMP-1 in breast cancer via advanced contrastive learning and structural attention.Molecular diversity · 2026Article
- Ubiquitination and NOncology letters · 2026Review
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Authors and funding
11 authors.
Funding
Abstract
backgroundRecurrence and metastasis remain the primary causes of treatment failure in nasopharyngeal carcinoma (NPC). This study aims to explore the functional role and regulatory mechanisms of peroxidasin (PXDN) in NPC progression.
methodsWeighted gene co-expression network analysis was performed to screen the module most relevant to the malignant progression of NPC from our internal cohort (Fujian cohort 1, N = 192), from which the PXDN was identified as the key molecule. Clinical significance of PXDN was assessed in the GEO database and NPC tissue microarrays from Fujian cohort 2 (N = 103). Functional experiments were used to determine the biological role of PXDN in NPC. Methylated RNA immunoprecipitation sequencing was used to identify PXDN N6-methyladenosine (m6A) modification site, and verified by a dual-luciferase reporter gene assay. RNA immunoprecipitation, RNA stability assay, and RNA pull-down assay were used to verify the relationship between PXDN and YTHDF1. The CRISPR/Cas9 system was used to disrupt the m⁶A motif in the PXDN gene to further validate its role. Next, transcriptome, proteomic analysis, and immunoprecipitation assay were conducted to assess downstream targets.
resultsPXDN was highly expressed in NPC and associated with poor prognosis. Suppression of PXDN drastically reduced proliferation, migration, invasion, and resistance to chemoradiation in vitro, concomitant with attenuated epithelial-mesenchymal transition. Knockdown of PXDN remarkably suppressed NPC tumorigenicity and liver metastasis in vivo. Mechanistically, PXDN promotes aggressiveness by extracellular matrix remodelling to activate the ITGB1-PI3K-AKT pathway. The aberrant expression of PXDN is governed by an m6A-based regulatory axis, wherein YTHDF1 recognizes WTAP-mediated PXDN m6A methylation to enhance its RNA stability and translation. Targeted specific demethylation of PXDN m6A by CRISPR/Cas9 system significantly decreased the expression of PXDN.
conclusionsWe reveal the crucial role of PXDN in driving NPC malignancy and the regulatory role of m6A methylation modification. Targeting PXDN expression or activity could be used to effectively control NPC progression.
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