Evidence map›Paper›PMID 27775089›Full record

ArticleScientific reports2016

Cell resistance to the Cytolethal Distending Toxin involves an association of DNA repair mechanisms.

Elisabeth Bezine, Yann Malaisé, Aurore Loeuillet, Marianne Chevalier, Elisa Boutet-Robinet, Bernard Salles, Gladys Mirey, Julien Vignard

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.2field-weighted citation impact, top 19% 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

22 citing papers in PubMed, 32 citations in OpenAlex.

  1. Cytolethal distending toxin enhancesInfection and immunity · 2026
    Article
  2. Review
  3. Review
  4. Cytolethal Distending Toxin EnhancesbioRxiv : the preprint server for biology · 2026
    Article
  5. Review
  6. Review
  7. Intratumoural microbiota: from theory to clinical application.Cell communication and signaling : CCS · 2023
    Review
  8. Review
  9. Review
  10. International journal of molecular sciences · 2022
    Article
  11. Review
  12. Review
  13. Article
  14. Article
  15. Article
  16. Functional Study ofToxins · 2020
    Article
  17. Review
  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.

Elisabeth BezineINRA, UMR1331, Toxalim, Research Center in Food Toxicology, F-31027 Toulouse, France.
Yann MalaiséINRA, UMR1331, Toxalim, Research Center in Food Toxicology, F-31027 Toulouse, France.
Aurore LoeuilletINRA, UMR1331, Toxalim, Research Center in Food Toxicology, F-31027 Toulouse, France.
Marianne ChevalierINRA, UMR1331, Toxalim, Research Center in Food Toxicology, F-31027 Toulouse, France.
Elisa Boutet-RobinetINRA, UMR1331, Toxalim, Research Center in Food Toxicology, F-31027 Toulouse, France.
Bernard SallesINRA, UMR1331, Toxalim, Research Center in Food Toxicology, F-31027 Toulouse, France.
Gladys MireyINRA, UMR1331, Toxalim, Research Center in Food Toxicology, F-31027 Toulouse, France.
Julien VignardINRA, UMR1331, Toxalim, Research Center in Food Toxicology, F-31027 Toulouse, France.
Toxalim Research Centre in Food Toxicology · FRUniversité Fédérale de Toulouse Midi-Pyrénées · FRUniversité Toulouse III - Paul Sabatier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Cytolethal Distending Toxin (CDT), produced by many bacteria, has been associated with various diseases including cancer. CDT induces DNA double-strand breaks (DSBs), leading to cell death or mutagenesis if misrepaired. At low doses of CDT, other DNA lesions precede replication-dependent DSB formation, implying that non-DSB repair mechanisms may contribute to CDT cell resistance. To address this question, we developed a proliferation assay using human cell lines specifically depleted in each of the main DNA repair pathways. Here, we validate the involvement of the two major DSB repair mechanisms, Homologous Recombination and Non Homologous End Joining, in the management of CDT-induced lesions. We show that impairment of single-strand break repair (SSBR), but not nucleotide excision repair, sensitizes cells to CDT, and we explore the interplay of SSBR with the DSB repair mechanisms. Finally, we document the role of the replicative stress response and demonstrate the involvement of the Fanconi Anemia repair pathway in response to CDT. In conclusion, our work indicates that cellular survival to CDT-induced DNA damage involves different repair pathways, in particular SSBR. This reinforces a model where CDT-related genotoxicity primarily involves SSBs rather than DSBs, underlining the importance of cell proliferation during CDT intoxication and pathogenicity.

Indexed as

Bacterial ToxinsDNA Breaks, Double-StrandedDNA End-Joining RepairDNA ReplicationHCT116 CellsHeLa CellsHomologous RecombinationHumansBacterial Toxinscytolethal distending toxin

Identifiers

PMID27775089
PMCPMC5075911
OpenAlexW2532933930

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.