ArticleBritish journal of cancer2025
Regulatory non-coding somatic mutations as drivers of neuroblastoma.
Article in British journal of cancer, 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.
- The Non-Coding rs5945619 Variant at Xp11.22 and Its Putative Regulatory Effects on Nearby Genes in Ecuadorian Mestizo Women with Breast Cancer: A Case Series and In Silico Cis-eQTL Analysis.International journal of molecular sciences · 2026Article
- Rho GTPases signaling mediates aggressiveness and differentiation in neuroblastoma tumors.Cell communication and signaling : CCS · 2026Article
- Third-generation whole-genome sequencing reveals the role of CNTNAP2 as a tumor suppressor gene in high-risk neuroblastomas.Journal of translational medicine · 2026Article
- Tumor suppressor network dysregulation in neuroblastoma: molecular mechanisms and precision therapeutic opportunities.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
backgroundEmerging evidence suggests that non-coding somatic single nucleotide variants (SNVs) in cis-regulatory elements (CREs) contribute to cancer by disrupting gene expression networks. However, the role of non-coding SNVs in cancer, particularly neuroblastoma, remains largely unclear.
methodsSNVs effect on CREs activity was evaluated by luciferase assays. Motif analysis and ChIP-qPCR experiments were employed to reveal the transcription factors (TFs) involved in these processes. We exploited CRISPR-Cas9 experiments to elucidate the role of these SNVs on the CREs target genes expression. Cell proliferation and invasion assays were performed to assess their role in neuroblastoma tumorigenesis.
resultsOur findings demonstrate that non-coding SNVs modify the transcriptional activity of two CREs altering the binding of STAT3 and SIN3A. Therefore, these SNVs reduce the expression of CTTNBP2 and MCF2L. We demonstrate that these two genes act as tumor suppressor in neuroblastoma. These pathogenetic SNVs may serve as oncogenic drivers by impairing the transcriptional programs essential for neuronal development and differentiation in which both the investigated TFs and target genes are involved.
conclusionOverall, the understanding of the functional role of non-coding variants elucidates their impact on tumorigenesis and can uncover new potential targets of cancer therapeutic strategies.
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