ArticleCancer management and research2025
Neuropilin-2 Mediates Radioresistance in Nasopharyngeal Carcinoma via Wnt/β-Catenin Pathway.
Article in Cancer management and research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Discovery and Cryo-EM-Guided Development of a Neuropilin-2-Binding Aptamer for Receptor Antagonism.Journal of the American Chemical Society · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: Neuropilin-2 (NRP2) is linked to poor prognosis in several malignant tumors. We elucidated the role of NRP2 in radiation resistance in nasopharyngeal carcinoma (NPC) and the underlying molecular pathways. Material and Methods: CNE-2R cells of NPC were used for NRP2 knockdown. Stable NRP2 knockdown was achieved using three siRNAs targeting distinct regions of the NRP2 gene. The effect of NRP2 knockdown was confirmed through qPCR for mRNA and Western blot (WB) for protein levels. Assays for cell viability and colony formation were conducted to assess cellular responses to NRP2 knockdown and ionizing radiation. Bioinformatics analyses, including differential expression and pathway enrichment using GEO datasets and GSEA analysis, were performed to elucidate the molecular mechanisms underlying NRP2 function. Results: After NRP2 knockdown in CNE-2R cells, NRP2 expression was significantly lower compared to non-knockdown cells by qPCR and Western blot analysis. NRP2 downregulation in CNE-2R cells led to decreased proliferation and clonal numbers post-radiation in comparison to the control group (P < 0.001). Analysis of the GEO database exhibited that NRP2 expression was notably elevated in nasopharyngeal carcinoma tissues vs normal tissues (p = 0.012). GSEA analysis showed a notable enhancement of the Wnt/β-catenin signaling pathway in NPC, with NES = 1.647, p adjust = 0.049, and FDR = 0.038. The WB analysis indicated that NRP2 knockdown notably reduced the level of WNT3a, Axin2, Cyclin D1, p-GSK3β, and β-catenin in the Wnt/β-catenin pathway in comparison to the negative control group (p < 0.05), with GSK3β expression remaining unchanged. Conclusion: NRP2 is connected with radioresistance in NPC, potentially via Wnt/β-catenin pathway, and may be a potential therapeutic target.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.