ArticleNature genetics2023
Cohesin maintains replication timing to suppress DNA damage on cancer genes.
Article in Nature genetics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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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.
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Who cites it
20 citing papers in PubMed, 28 citations in OpenAlex.
- Folding a broken genome: the versatile roles of cohesin in genome maintenance.Nature reviews. Genetics · 2026Review
- RAD21 regulation of the enhancer-promoter chromatin loop of RAD51 promotes PARPi resistance in ovarian cancer.Journal of translational medicine · 2026Article
- Decoding DNA metabolism and its clinical relevance through the lens of high-throughput sequencing assays.Medical review (2021) · 2026Review
- Cohesin extrudes chromatin loop unidirectionally through two modes of mechanisms in human cells.bioRxiv : the preprint server for biology · 2026Article
- CTCF/cohesin-binding sites are susceptible to replication-associated DNA damage and genomic instability in cancer cells.iScience · 2026Article
- Interplay between cohesin and RNA polymerase II in regulating chromatin interactions and gene transcription.Nature structural & molecular biology · 2026Article
- S-phase PARylation of microprotein RSMC enhances the function of Sororin in sister chromatid cohesion.The EMBO journal · 2026Article
- Qingre Huoxue decoction and its active compound Quercetin modulate bone remodeling by inhibiting ATF4 hyperactivation to attenuate bone erosion in rheumatoid arthritis.Journal of orthopaedic surgery and research · 2025Article
- The Biological Function of Genome Organization.International journal of molecular sciences · 2025Review
- Unraveling the cohesin-chromatin interface: identifying protein interactions that modulate chromosome structure and function.Epigenetics & chromatin · 2025Article
- Barrier effects on the kinetics of cohesin-mediated loop extrusion.Biophysical journal · 2025Article
- Review
- The double life of mammalian DNA replication origins.Genes & development · 2025Review
- Article
- KMT2C/KMT2D-dependent H3K4me1 mediates changes in DNA replication timing and origin activity during a cell fate transition.Cell reports · 2025Article
- Nuclear Overexpression of SAMHD1 Induces M Phase Stalling in Hepatoma Cells and Suppresses HCC Progression by Interacting with the Cohesin Complex.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- A dual role of Cohesin in DNA DSB repair.Nature communications · 2025Article
- Review
- Cohesin mutations in acute myeloid leukemia.Leukemia · 2024Review
- PHF2 regulates genome topology and DNA replication in neural stem cells via cohesin.Nucleic acids research · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cohesin loss-of-function mutations are frequently observed in tumors, but the mechanism underlying its role in tumorigenesis is unclear. Here, we found that depletion of RAD21, a core subunit of cohesin, leads to massive genome-wide DNA breaks and 147 translocation hotspot genes, co-mutated with cohesin in multiple cancers. Increased DNA damages are independent of RAD21-loss-induced transcription alteration and loop anchor disruption. However, damage-induced chromosomal translocations coincide with the asymmetrically distributed Okazaki fragments of DNA replication, suggesting that RAD21 depletion causes replication stresses evidenced by the slower replication speed and increased stalled forks. Mechanistically, approximately 30% of the human genome exhibits an earlier replication timing after RAD21 depletion, caused by the early initiation of >900 extra dormant origins. Correspondingly, most translocation hotspot genes lie in timing-altered regions. Therefore, we conclude that cohesin dysfunction causes replication stresses induced by excessive DNA replication initiation, resulting in gross DNA damages that may promote tumorigenesis.
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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 Socratic graph.