Evidence map›Paper›PMID 28881569›Full record

ArticleOncotarget2017

Aurora A kinase regulates non-homologous end-joining and poly(ADP-ribose) polymerase function in ovarian carcinoma cells.

Thuy-Vy Do, Jeff Hirst, Stephen Hyter, Katherine F Roby, Andrew K Godwin

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

34 citing papers in PubMed, 44 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Selective Aurora A-TPX2 Interaction Inhibitors HaveJournal of medicinal chemistry · 2024
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Combined TRIP13 and Aurora Kinase Inhibition Induces Apoptosis in Human Papillomavirus-Driven Cancers.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022
    Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

5 authors at 2 institutions in 1 country.

Thuy-Vy DoDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA.
Jeff HirstDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA.
Stephen HyterDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA.
Katherine F RobyAnatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS, USA.
Andrew K GodwinDepartment of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS, USA.
University of Kansas Medical Center · USThe University of Kansas Cancer Center · US

Funding

Transgenic & Gene-Targeting Shared ResourceP30CA168524 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI ROY A. JENSEN · 2012 to 2026
$40.1M
Novel Approaches for the Control of Microbial PathogensP30GM103326 · NIGMS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI LUTKENHAUS, JOSEPH F · 2012 to 2016
$5.3M
Exploiting Biological Networks to Improve Clinical Treatment of Ovarian CancerR01CA140323 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI GODWIN, ANDREW K. · 2010 to 2014
$2.1M
Targeting Kinesin Family Member 15 for the Treatment of CancerR01CA214545 · NCI · UNIVERSITY OF KANSAS MEDICAL CENTER · PI GODWIN, ANDREW K., ROY, ANURADHA · 2017 to 2019
$1.8M
NCI NIH HHS P30 CA168524NCI NIH HHS R01 CA140323NCI NIH HHS R01 CA214545NIGMS NIH HHS P30 GM103326
6 · The paper itself

Abstract

Ovarian cancer is usually diagnosed at late stages when cancer has spread beyond the ovary and patients ultimately succumb to the development of drug-resistant disease. There is an urgent and unmet need to develop therapeutic strategies that effectively treat ovarian cancer and this requires a better understanding of signaling pathways important for ovarian cancer progression. Aurora A kinase (AURKA) plays an important role in ovarian cancer progression by mediating mitosis and chromosomal instability. In the current study, we investigated the role of AURKA in regulating the DNA damage response and DNA repair in ovarian carcinoma cells. We discovered that AURKA modulated the expression and activity of PARP, a crucial mediator of DNA repair that is a target of therapeutic interest for the treatment of ovarian and other cancers. Further, specific inhibition of AURKA activity with the small molecule inhibitor, alisertib, stimulated the non-homologous end-joining (NHEJ) repair pathway by elevating DNA-PKcs activity, a catalytic subunit required for double-strand break (DSB) repair, as well as decreased the expression of PARP and BRCA1/2, which are required for high-fidelity homologous recombination-based DNA repair. Further, AURKA inhibition stimulates error-prone NHEJ repair of DNA double-strand breaks with incompatible ends. Consistent with

Indexed as

alisertibAurora A kinasedouble-strand breakovarian cancerPARP

Identifiers

PMID28881569
PMCPMC5584138
OpenAlexW2734284818

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.