Evidence map›Paper›PMID 21378315›Full record

ArticleAnticancer research2011

Apurinic/Apyrimidinic endonuclease 1 regulates inflammatory response in macrophages.

Andrej Jedinak, Shailesh Dudhgaonkar, Mark R Kelley, Daniel Sliva

Abstract read
In one paragraph

Article in Anticancer research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.6field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. The APE1/REF-1 and the hallmarks of cancer.Molecular biology reports · 2024
    Review
  8. Review
  9. Article
  10. Beyond VEGF: Targeting Inflammation and Other Pathways for Treatment of Retinal Disease.The Journal of pharmacology and experimental therapeutics · 2023
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. Article
  19. Article
  20. APE1/Ref-1 as a Novel Target for Retinal Diseases.Journal of cellular signaling · 2021
    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

4 authors at 1 institution in 1 country.

Andrej JedinakCancer Research Laboratory, Methodist Research Institute, Indiana University Health, 1800 N Capitol Ave, E504, Indianapolis, IN 46202, USA.
Shailesh Dudhgaonkar
Mark R Kelley
Daniel Sliva
Indiana University – Purdue University Indianapolis · US

Funding

The Role of Ape1 in Neurotoxicity of Cancer TreatmentsR01CA121168 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI KELLEY, MARK R. · 2008 to 2012
$2.4M
Imbalancing DNA BER to enhance Ovarian Tumor SensitivityR01CA106298 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KELLEY, MARK R. · 2004 to 2008
$1.5M
Mechanism of Redox Regulation by Ape1/Ref-1R01CA114571 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI GEORGIADIS, MILLIE M · 2006 to 2010
$1.2M
Therapeutic/Mechanistic Role of Ape1 in Germ Cell TumorsR01CA094025 · NCI · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI KELLEY, MARK R. · 2003 to 2007
$1.1M
NCI NIH HHS CA106298NCI NIH HHS CA114571NCI NIH HHS CA121168NCI NIH HHS CA94025NCI NIH HHS R01 CA094025NCI NIH HHS R01 CA106298NCI NIH HHS R01 CA114571NCI NIH HHS R01 CA121168
6 · The paper itself

Abstract

The multi-functional apyrimidinic endonuclease 1/redox factor-1 (APE1/Ref-1) DNA repair and redox signaling protein has been shown to have a role in cancer growth and survival, however, little has been investigated concerning its role in inflammation. In this study, an APE1 redox-specific inhibitor (E3330) was used in lypopolysaccharide (LPS)-stimulated macrophages (RAW264.7). E3330 clearly suppressed secretion of inflammatory cytokines including tumor necrosis factor-α (TNF-α), interleukin (IL-6) and IL-12 and inflammatory mediators nitric oxide (NO) as well as prostaglandin E(2) (PGE(2)) from the LPS-stimulated RAW264.7 cells. These data were supported by the down-regulation of the LPS-dependent expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) genes in the RAW264.7 cells. The effects of E3330 were mediated by the inhibition of transcription factors nuclear factor-κB (NF-κB) and activator protein 1 (AP-1) in the LPS-stimulated macrophages, both known targets of APE1. In conclusion, pharmacological inhibition of APE1 by E3330 suppresses inflammatory response in activated macrophages and can be considered as a novel therapeutic strategy for the inhibition of tumor-associated macrophages.

Indexed as

AnimalsAnti-Inflammatory Agents, Non-SteroidalBenzoquinonesCells, CulturedCyclooxygenase 2DinoprostoneDNA-(Apurinic or Apyrimidinic Site) LyaseLipopolysaccharidesMacrophagesMiceNF-kappa BNitric OxideNitric Oxide Synthase Type IIOxidation-ReductionPropionatesSignal TransductionAnti-Inflammatory Agents, Non-SteroidalApex1 protein, mouseBenzoquinonesCyclooxygenase 2DinoprostoneDNA-(Apurinic or Apyrimidinic Site) LyaseE 3330LipopolysaccharidesNF-kappa BNitric OxideNitric Oxide Synthase Type IINos2 protein, mousePropionatesPtgs2 protein, mouseTranscription Factor AP-1Tumor Necrosis Factor-alpha

Identifiers

PMID21378315
PMCPMC3256557
OpenAlexW1862480368

What OpenQuestion holds

Textmetadata
LicenceTDM
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.