ArticleLife science alliance2023
BAZ2A-RNA mediated association with TOP2A and KDM1A represses genes implicated in prostate cancer.
Article in Life science alliance, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- ATP-dependent chromatin remodelers in prostate cancer progression and therapeutic resistance.Endocrinology · 2026Review
- Hesperidin and Hesperetin: Epigenetic-Stemness Crosstalk, Antitumor Mechanisms, Preclinical Data and Translation Barriers.Biomolecules · 2026Review
- Comparative Phosphoproteomic Profiling and Network-based Interactome Analysis of GRK5 and GRK6.Cell biochemistry and biophysics · 2026Article
- Prediction of Prostate Adenocarcinoma Recurrence Prognosis and Immune Status Through 6-Acetoxy-Anopterine Resistance-Associated Programmed Cell Death Genes.Cancer management and research · 2026Article
- Alternative Splicing in Tumorigenesis and Cancer Therapy.Biomolecules · 2025Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BAZ2A represses rRNA genes (rDNA) that are transcribed by RNA polymerase I. In prostate cancer (PCa), BAZ2A function goes beyond this role because it represses genes frequently silenced in metastatic disease. However, the mechanisms of this BAZ2A-mediated repression remain elusive. Here, we show that BAZ2A represses genes through its RNA-binding TAM domain using mechanisms differing from rDNA silencing. Although the TAM domain mediates BAZ2A recruitment to rDNA, in PCa, this is not required for BAZ2A association with target genes. Instead, the BAZ2A-TAM domain in association with RNA mediates the interaction with topoisomerase 2A (TOP2A) and histone demethylase KDM1A, whose expression positively correlates with BAZ2A levels in localized and metastatic PCa. TOP2A and KDM1A pharmacological inhibition up-regulate BAZ2A-repressed genes that are regulated by inactive enhancers bound by BAZ2A, whereas rRNA genes are not affected. Our findings showed a novel RNA-based mechanism of gene regulation in PCa. Furthermore, we determined that RNA-mediated interactions between BAZ2A and TOP2A and KDM1A repress genes critical to PCa and may prove to be useful to stratify prostate cancer risk and treatment in patients.
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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.