ArticleThe Journal of cell biology2025
Epigenetic deprogramming by disruption of CIZ1-RNA nuclear assemblies in early-stage breast cancers.
Article in The Journal of cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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
4 citing papers in PubMed.
- CIZ1 regulates G1 length and the CDK threshold for initiation of DNA replication to prevent DNA replication stress.Nucleic acids research · 2026Article
- Using combined RNA/DNA short read sequencing to investigate allele-specific expression from the inactive X chromosome in human cells.bioRxiv : the preprint server for biology · 2026Article
- AURKB-driven dissolution of CIZ1-RNA assemblies from the inactive X chromosome in mitosis.Nucleic acids research · 2026Article
- Molecular Insights into Phytochemicals Mediated Epigenetic Regulation in Preclinical Models of Breast Cancer.Drug design, development and therapy · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
CIZ1 is part of the RNA-dependent supramolecular assemblies that form around the inactive X-chromosome (Xi) in female cells and smaller assemblies throughout the nucleus in both sexes. Here, we show that CIZ1 C-terminal anchor domain (AD) is elevated in human breast tumor transcriptomes, even at stage I. Elevation correlates with deprotection of chromatin and upregulation of lncRNA-containing gene clusters in ∼10 Mb regions enriched in cancer-associated genes. We modeled the effect of AD on endogenous CIZ1-Xi assemblies and observed dominant-negative interference with their reformation after mitosis, leading to abnormal assemblies similar to those in breast cancer cells, and depletion of H2AK119ub1, H3K27me3, and Xist. Consistent alterations in gene expression were evident across the genome, showing that AD-mediated interference has a destabilizing effect, likely by unscheduled exposure of underlying chromatin to modifying enzymes. The data argue for a dominant, potent, and rapid effect of CIZ1 AD that can deprogram gene expression patterns and which may predispose incipient tumors to epigenetic instability.
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.