ArticleMolecular therapy : the journal of the American Society of Gene Therapy2021
Recurrent ZNF83-E293V Mutation Promotes Bladder Cancer Progression through the NF-κB Pathway via Transcriptional Dysregulation of S100A8.
Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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24 citing papers in PubMed, 55 citations in OpenAlex.
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- Exploratory analysis of a Novel RACK1 mutation and its potential role in epileptic seizures via Microglia activation.Journal of neuroinflammation · 2025Article
- S100A8 promotes the proliferation, migration and invasion in bladder cancer cells.Journal of Cancer · 2025Article
- CCN1 Promotes Mesenchymal Phenotype Transition Through Activating NF-κB Signaling Pathway Regulated by S100A8 in Glioma Stem Cells.CNS neuroscience & therapeutics · 2024Article
- A Catalogue of Structural Variation across Ancestrally Diverse Asian Genomes.Nature communications · 2024Article
- Novel therapeutic targets: bifidobacterium-mediated urea cycle regulation in colorectal cancer.Cell biology and toxicology · 2024Article
- Dysregulated RNA editing of EIF2AK2 in polycystic ovary syndrome: clinical relevance and functional implications.BMC medicine · 2024Article
- Development of a prognostic signature for immune-associated genes in bladder cancer and exploring potential drug findings.International urology and nephrology · 2024Article
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Authors and funding
19 authors at 7 institutions in 2 countries.
Funding
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Abstract
Urothelial carcinoma (UC) is the predominant form of bladder cancer. Significant molecular heterogeneity caused by diverse molecular alterations brings about large variations in the response to treatment in UC. An improved understanding of the genetic mechanisms underlying the development and progression of UC is essential. Through deep analysis of next-generation sequencing data of 99 UC patients, we found that 18% of cases had recurrent somatic mutations in zinc finger protein gene zinc finger protein 83 (ZNF83). ZNF83 mutations were correlated with poor prognosis of UC. We also found a hotspot mutation, p.E293V, in the evolutionarily well-conserved region of ZNF83. ZNF83-E293V increased tumor growth and reduced the apoptosis of UC cells compared to wild-type ZNF83 both in vitro and in mice xenografted tumors. ZNF83-E293V activated nuclear factor κB (NF-κB) more potently than did the wild-type protein owing to its decreased transcriptional repression for S100A8. The NF-κB inhibitors could pharmacologically block the tumor growth in mice engrafted with ZNF83-E293V-transfected UC cells. These findings provide a mechanistic insight and a potential therapeutic strategy for UC, which established a foundation for using the ZNF83-E293V mutation as a predictive biomarker of therapeutic response from NF-κB inhibitors.
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