Evidence map›Paper›PMID 27109102›Full record

ArticleOncogene2016

NCOA3 coactivator is a transcriptional target of XBP1 and regulates PERK-eIF2α-ATF4 signalling in breast cancer.

A Gupta, M M Hossain, N Miller, M Kerin, G Callagy, S Gupta

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.5field-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

40 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. TIGAR Suppresses ER Stress-Induced Neuronal Injury through Targeting ATF4 Signaling in Cerebral Ischemia/Reperfusion.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  10. Review
  11. Review
  12. Article
  13. Roles of X-box binding protein 1 in liver pathogenesis.Clinical and molecular hepatology · 2025
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
  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

6 authors at 1 institution in 1 country.

A GuptaDiscipline of Pathology, School of Medicine, Lambe Institute for Translational Research, National University of Ireland, Galway, Ireland.
M M HossainDiscipline of Pathology, School of Medicine, Lambe Institute for Translational Research, National University of Ireland, Galway, Ireland.
N MillerDiscipline of Surgery, School of Medicine, Clinical Science Institute, National University of Ireland, Galway, Ireland.
M KerinDiscipline of Surgery, School of Medicine, Clinical Science Institute, National University of Ireland, Galway, Ireland.
G CallagyDiscipline of Pathology, School of Medicine, Lambe Institute for Translational Research, National University of Ireland, Galway, Ireland.
S GuptaDiscipline of Pathology, School of Medicine, Lambe Institute for Translational Research, National University of Ireland, Galway, Ireland.
Ollscoil na Gaillimhe – University of Galway · IE

Funding

Breast Cancer Now 2011MAYPR26
6 · The paper itself

Abstract

XBP1 is a multitasking transcription factor and a key component of the unfolded protein response (UPR). Despite the wealth of knowledge about the role of XBP1 in luminal/ER-positive breast cancer, not much is known about the effectors of XBP1 in this context. Here we show that NCOA3 is a transcriptional target of XBP1. We observed increased expression of NCOA3 during conditions of UPR and oestrogen (E2) stimulation. Further investigations revealed a role for the IRE1-XBP1 axis in the induction of NCOA3 during UPR and oestrogen signalling. We identify a novel role for NCOA3 in activation of PERK-ATF4 axis during UPR where knockdown of NCOA3 compromised the optimal activation of the PERK-ATF4 pathway. We found that NCOA3 is required for induction of XBP1 during E2 stimulation and uncover a positive feedback regulatory loop that maintains high levels of NCOA3 and XBP1 in breast cancer. Furthermore, upregulated NCOA3 was required for XBP1-mediated resistance to antihormonal agents. Increased expression of NCOA3 was associated with poor prognosis and higher levels of XBP1-S in breast cancer tissues. Our results uncover a novel steroid hormone-independent role for NCOA3 in UPR signalling. Further we identify a positive feedback regulatory loop consisting of XBP1 and NCOA3 that maintains high levels of NCOA3 and XBP1 expression in breast cancer tissues. Taken together our data identify XBP1-NCOA3 axis that regulates cell fate decisions in ER-positive breast cancer cells.

Indexed as

Gene Expression Regulation, NeoplasticSignal TransductionActivating Transcription Factor 4Breast NeoplasmsCell Line, TumoreIF-2 KinaseEndoplasmic Reticulum StressEndoribonucleasesEukaryotic Initiation Factor-2FemaleHumansNuclear Receptor Coactivator 3PrognosisProtein Serine-Threonine KinasesRNA, MessengerTranscription, GeneticActivating Transcription Factor 4EIF2AK3 protein, humaneIF-2 KinaseEndoribonucleasesERN1 protein, humanEukaryotic Initiation Factor-2NCOA3 protein, humanNuclear Receptor Coactivator 3Protein Serine-Threonine KinasesRNA, MessengerX-Box Binding Protein 1

Identifiers

PMID27109102
PMCPMC4979996
OpenAlexW2342388613

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.