Evidence map›Paper›PMID 42342951›Full record

ArticleNature cell biology2026

Cis and trans regulatory mechanisms of extrachromosomal DNA segregation.

Yipeng Xie, Jun Yi Stanley Lim, Wenyue Liu, Collin Gilbreath, Xiaohui Sun, Kailiang Qiao, Yoon Jung Kim, Sihan Wu

Abstract read
In one paragraph

Article in Nature cell biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

  • Update of
    2026
5 · Who and what money

Authors and funding

8 authors.

Yipeng XieChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID http://orcid.org/0000-0002-7454-126X
Jun Yi Stanley LimChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Wenyue LiuDepartment of Cell Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Collin GilbreathChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.ORCID http://orcid.org/0000-0002-8683-983X
Xiaohui SunChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Kailiang QiaoChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA.
Yoon Jung KimChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA. Yoonjung.kim@utsouthwestern.edu.ORCID http://orcid.org/0000-0002-2942-294X
Sihan WuChildren's Medical Center Research Institute, University of Texas Southwestern Medical Center, Dallas, TX, USA. Sihan.wu@utsouthwestern.edu.ORCID http://orcid.org/0000-0001-8329-7492

Funding

eDyNAmiC-TEXASSWOT2CA278683 · NCI · UT SOUTHWESTERN MEDICAL CENTER · PI Zhijian J Chen · 2022 to 2026
$2.4M
American Cancer Society (American Cancer Society, Inc.) CAT-24-1379043-01-CATCancer Prevention and Research Institute of Texas (Cancer Prevention Research Institute of Texas) RP210041Cancer Prevention and Research Institute of Texas (Cancer Prevention Research Institute of Texas) RR210034Cancer Research UK (CRUK) CGCATF-2021/100023NCI NIH HHS OT2 CA278683U.S. Department of Health & Human Services | NIH | NCI | Division of Cancer Epidemiology and Genetics, National Cancer Institute (National Cancer Institute Division of Cancer Epidemiology and Genetics) OT2CA278683
6 · The paper itself

Abstract

Extrachromosomal DNAs (ecDNAs) attach to chromosomes during mitosis for random segregation and promote cancer heterogeneity. However, the mechanism governing ecDNA-chromosome mitotic interactions remains poorly understood. Here we show that ecDNAs tether to histone H3 lysine 27 acetylation (H3K27ac)-marked chromatin during mitosis. Depleting H3K27ac disrupts this interaction. Diverse bromodomain proteins, as H3K27ac readers, stabilize ecDNA-chromosome binding in a context-dependent and complementary manner. Although disrupting the Mediator complex in asynchronous cells detaches ecDNAs from mitotic chromosomes, Mediator and active Pol II are absent from ecDNAs during mitosis, suggesting that ecDNAs are transcriptionally silent during mitosis. Instead, inactive Pol II mediates ecDNA attachment. Furthermore, CRISPR interference targeting transcriptional regulatory elements on ecDNA impairs ecDNA segregation. Mis-segregated ecDNAs were expelled into the cytosol, leading to diminished oncogene expression and a reversal of therapy resistance. Our research provides universal cis and trans regulatory mechanisms of ecDNA segregation, offering deeper insight into ecDNA-driven oncogenesis.

Indexed as

Chromosome SegregationExtrachromosomal DNAMitosisAcetylationChromatinDNA Polymerase IIHistonesHumansChromatinDNA Polymerase IIExtrachromosomal DNAHistones

Identifiers

PMID42342951
PMCPMC13364683

What OpenQuestion holds

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Registered trials

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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.