Evidence map›Paper›PMID 23786772›Full record

ArticleCancer research2013

Transcription poisoning by Topoisomerase I is controlled by gene length, splice sites, and miR-142-3p.

Stéphanie Solier, Michael C Ryan, Scott E Martin, Sudhir Varma, Kurt W Kohn, Hongfang Liu, Barry R Zeeberg, Yves Pommier

Open access · hybridAbstract read
In one paragraph

Article in Cancer research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.3field-weighted citation impact, top 7% of its field
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

35 citing papers in PubMed, 49 citations in OpenAlex.

  1. Article
  2. The Roles of Topoisomerases in Transcriptional Regulation.International journal of molecular sciences · 2026
    Review
  3. Dynamic Supercoiling Sponsors Transcription Amplification by MYC.bioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. The DNA damage response to transcription stress.Nature reviews. Molecular cell biology · 2019
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Topoisomerases as anticancer targets.The Biochemical journal · 2018
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Stéphanie SolierLaboratory of Molecular Pharmacology, Center for Cancer Research, National Cancer Institute; NIH Center for Advancing Translational Sciences, Bethesda, MD 20892-4255, USA.
Michael C Ryan
Scott E Martin
Sudhir Varma
Kurt W Kohn
Hongfang Liu
Barry R Zeeberg
Yves Pommier
In Silico Biosciences (United States) · USCenter for Cancer Research · USNational Cancer Institute · US

Funding

DNA Topoisomerases as Target of Action of Anticancer DrugsZIABC006161 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 2009 to 2025
$16.8M
DNA TOPOISOMERASES AS TARGET OF ACTION OF ANTICANCER DRUGSZ01BC006161 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI POMMIER, YVES · 1996 to 2008
$1.5M
Intramural NIH HHS Z01 BC006161
6 · The paper itself

Abstract

Topoisomerase I (Top1) relaxes DNA supercoiling by forming transient cleavage complexes (Top1cc) up- and downstream of transcription complexes. Top1cc can be trapped by carcinogenic and endogenous DNA lesions and by camptothecin, resulting in transcription blocks. Here, we undertook genome-wide analysis of camptothecin-treated cells at exon resolution. RNA samples from HCT116 and MCF7 cells were analyzed with the Affy Exon Array platform, allowing high-resolution mapping along 18,537 genes. Long genes that are highly expressed were the most susceptible to downregulation, whereas short genes were preferentially upregulated. Along the body of genes, downregulation was most important toward the 3'-end and increased with the number of exon-intron junctions. Ubiquitin and RNA degradation-related pathway genes were selectively downregulated. Parallel analysis of microRNA with the Agilent miRNA microarray platform revealed that miR-142-3p was highly induced by camptothecin. More than 10% of the downregulated genes were targets of this p53-dependent microRNA. Our study shows the profound impact of Top1cc on transcription elongation, especially at intron-exon junctions and on transcript stability by microRNA miR-142-3p upregulation.

Indexed as

CamptothecinCell Line, TumorDNA Topoisomerases, Type IGene Expression RegulationHCT116 CellsHumansMicroRNAsOligonucleotide Array Sequence AnalysisReverse Transcriptase Polymerase Chain ReactionRNA, Small InterferingRNA SplicingTopoisomerase I InhibitorsTranscription, GeneticTransfectionCamptothecinDNA Topoisomerases, Type IMicroRNAsMIRN142 microRNA, humanRNA, Small InterferingTopoisomerase I Inhibitors

Identifiers

PMID23786772
PMCPMC3874869
OpenAlexW2117088118

What OpenQuestion holds

Textmetadata
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Read underepoch 390

Registered trials

None linked

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.