Evidence map›Paper›PMID 36819096›Full record

ArticleFrontiers in cell and developmental biology2023

OGG1 competitive inhibitors show important off-target effects by directly inhibiting efflux pumps and disturbing mitotic progression.

Xhaferr Tanushi, Guillaume Pinna, Marie Vandamme, Capucine Siberchicot, Ostiane D'Augustin, Anne-Marie Di Guilmi, J Pablo Radicella, Bertrand Castaing, Rebecca Smith, Sebastien Huet and 2 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.8field-weighted citation impact, top 13% 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

4 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025
    Review
  3. Review
  4. Review
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

12 authors at 8 institutions in 1 country.

Xhaferr TanushiUniversité Paris-Saclay, CEA/IBFJ/IRCM. UMR Stabilité Génétique Cellules Souches et Radiations, Fontenay-aux-Roses, France.
Guillaume PinnaUniversité Paris-Saclay, Inserm, CEA/IBFJ/IRCM/Plateforme PARi, UMR Stabilité Génétique Cellules Souches et Radiations, Fontenay-aux-Roses, France.
Marie VandammeUniversité Paris-Saclay, Inserm, CEA/IBFJ/IRCM/Plateforme PARi, UMR Stabilité Génétique Cellules Souches et Radiations, Fontenay-aux-Roses, France.
Capucine SiberchicotUniversité Paris-Saclay, CEA/IBFJ/IRCM. UMR Stabilité Génétique Cellules Souches et Radiations, Fontenay-aux-Roses, France.
Ostiane D'AugustinUniversité Paris-Saclay, CEA/IBFJ/IRCM. UMR Stabilité Génétique Cellules Souches et Radiations, Fontenay-aux-Roses, France.
Anne-Marie Di GuilmiUniversité Paris-Saclay, CEA/IBFJ/IRCM. UMR Stabilité Génétique Cellules Souches et Radiations, Fontenay-aux-Roses, France.
J Pablo RadicellaUniversité Paris-Saclay, CEA/IBFJ/IRCM. UMR Stabilité Génétique Cellules Souches et Radiations, Fontenay-aux-Roses, France.
Bertrand CastaingCentre de Biophysique Moléculaire (CBM) UPR4301 CNRS, Université d'Orléans, Orléans, France.
Rebecca SmithUniversité Rennes, CNRS, IGDR (Institut de Génétique et Développement de Rennes)-UMR 6290, BIOSIT-UMS 3480, Rennes, France.
Sebastien HuetUniversité Rennes, CNRS, IGDR (Institut de Génétique et Développement de Rennes)-UMR 6290, BIOSIT-UMS 3480, Rennes, France.
François LeteurtreUniversité Paris-Saclay, CEA/IBFJ/IRCM. UMR Stabilité Génétique Cellules Souches et Radiations, Fontenay-aux-Roses, France.
Anna CampalansUniversité Paris-Saclay, CEA/IBFJ/IRCM. UMR Stabilité Génétique Cellules Souches et Radiations, Fontenay-aux-Roses, France.
Université Paris-Saclay · FRCEA Paris-Saclay - Etablissement de Fontenay-aux-roses · FRCommissariat à l'Énergie Atomique et aux Énergies Alternatives · FRCEA Paris-Saclay · FRInserm · FRInstitut de génétique et de développement de Rennes · FRInstitut Universitaire de France · FRUniversité d'Orléans · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

One of the most abundant DNA lesions induced by Reactive oxygen species (ROS) is 8-oxoG, a highly mutagenic lesion that compromises genetic instability when not efficiently repaired. 8-oxoG is specifically recognized by the DNA-glycosylase OGG1 that excises the base and initiates the Base Excision Repair pathway (BER). Furthermore, OGG1 has not only a major role in DNA repair but it is also involved in transcriptional regulation. Cancer cells are particularly exposed to ROS, thus challenging their capacity to process oxidative DNA damage has been proposed as a promising therapeutic strategy for cancer treatment. Two competitive inhibitors of OGG1 (OGG1i) have been identified, TH5487 and SU0268, which bind to the OGG1 catalytic pocket preventing its fixation to the DNA. Early studies with these inhibitors show an enhanced cellular sensitivity to cytotoxic drugs and a reduction in the inflammatory response. Our study uncovers two unreported off-targets effects of these OGG1i that are independent of OGG1.

Indexed as

8-oxoGBase Excision Repair (BER)OGG1OGG1 inhibitorSU0268TH5487

Identifiers

PMID36819096
PMCPMC9936318
OpenAlexW4319158015

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.