Evidence map›Paper›PMID 28414308›Full record

ArticleOncogene2017

Complex regulation of LCoR signaling in breast cancer cells.

S Jalaguier, C Teyssier, T Nait Achour, A Lucas, S Bonnet, C Rodriguez, N Elarouci, M Lapierre, V Cavaillès

Open access · hybridAbstract read
In one paragraph

Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  8. Article
  9. Review
  10. Article
  11. Article
  12. RIP140 regulatesCancer drug resistance (Alhambra, Calif.) · 2022
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Cholesterol, Oxysterols and LXRs in Breast Cancer Pathophysiology.International journal of molecular sciences · 2020
    Review
  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

9 authors at 2 institutions in 1 country.

S JalaguierIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
C TeyssierIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
T Nait AchourIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
A LucasIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
S BonnetIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
C RodriguezIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
N ElarouciProgramme Cartes d'Identité des Tumeurs (CIT), Ligue Nationale Contre Le Cancer, Paris, France.
M LapierreIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.ORCID 0000-0002-4708-805X
V CavaillèsIRCM, Institut de Recherche en Cancérologie de Montpellier, Montpellier, France.
Inserm · FRLa Ligue Contre le Cancer · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ligand-dependent corepressor (LCoR) is a transcriptional repressor of ligand-activated estrogen receptors (ERs) and other transcription factors that acts both by recruiting histone deacetylases and C-terminal binding proteins. Here, we first studied LCOR gene expression in breast cancer cell lines and tissues. We detected two mRNAs variants, LCoR and LCoR2 (which encodes a truncated LCoR protein). Their expression was highly correlated and localized in discrete nuclear foci. LCoR and LCoR2 strongly repressed transcription, inhibited estrogen-induced target gene expression and decreased breast cancer cell proliferation. By mutagenesis analysis, we showed that the helix-turn-helix domain of LCoR is required for these effects. Using in vitro interaction, coimmunoprecipitation, proximity ligation assay and confocal microscopy experiments, we found that receptor-interacting protein of 140 kDa (RIP140) is a LCoR and LCoR2 partner and that this interaction requires the HTH domain of LCoR and RIP140 N- and C-terminal regions. By increasing or silencing LCoR and RIP140 expression in human breast cancer cells, we then showed that RIP140 is necessary for LCoR inhibition of gene expression and cell proliferation. Moreover, LCoR and RIP140 mRNA levels were strongly correlated in breast cancer cell lines and biopsies. In addition, RIP140 positively regulated LCoR expression in human breast cancer cells and in transgenic mouse models. Finally, their expression correlated with overall survival of patients with breast cancer. Taken together, our results provide new insights into the mechanism of action of LCoR and RIP140 and highlight their strong interplay for the control of gene expression and cell proliferation in breast cancer cells.

Indexed as

Gene Expression Regulation, NeoplasticAdaptor Proteins, Signal TransducingAnimalsBiopsyBreast NeoplasmsCell Line, TumorCell ProliferationCohort StudiesCOS CellsFemaleHelix-Turn-Helix MotifsHumansKaplan-Meier EstimateMiceMice, TransgenicMutagenesisAdaptor Proteins, Signal TransducingLCOR protein, humanNRIP1 protein, humanNuclear ProteinsNuclear Receptor Interacting Protein 1Repressor Proteins

Identifiers

PMID28414308
PMCPMC5562849
OpenAlexW2606879338

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.