Evidence map›Paper›PMID 28051153›Full record

ArticleScientific reports2017

The metastasis suppressor RARRES3 as an endogenous inhibitor of the immunoproteasome expression in breast cancer cells.

Alison M Anderson, Murugan Kalimutho, Sarah Harten, Devathri M Nanayakkara, Kum Kum Khanna, Mark A Ragan

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. The Phospholipase AJournal of lipid and atherosclerosis · 2026
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  7. COMMD3 loss drives invasive breast cancer growth by modulating copper homeostasis.Journal of experimental & clinical cancer research : CR · 2023
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  8. Review
  9. Forward Genetics in Apicomplexa Biology: The Host Side of the Story.Frontiers in cellular and infection microbiology · 2022
    Review
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  17. Article
  18. Blockade of PDGFRβ circumvents resistance to MEK-JAK inhibition via intratumoral CD8Journal of experimental & clinical cancer research : CR · 2019
    Article
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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 2 institutions in 1 country.

Alison M AndersonInstitute for Molecular Bioscience, The University of Queensland, Brisbane QLD 4072, Australia.
Murugan KalimuthoSignal Transduction Laboratory, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, Brisbane QLD 4006, Australia.
Sarah HartenSignal Transduction Laboratory, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, Brisbane QLD 4006, Australia.
Devathri M NanayakkaraSignal Transduction Laboratory, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, Brisbane QLD 4006, Australia.
Kum Kum KhannaSignal Transduction Laboratory, QIMR Berghofer Medical Research Institute, 300 Herston Road, Herston, Brisbane QLD 4006, Australia.
Mark A RaganInstitute for Molecular Bioscience, The University of Queensland, Brisbane QLD 4072, Australia.
QIMR Berghofer Medical Research Institute · AUUniversity of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In breast cancer metastasis, the dynamic continuum involving pro- and anti-inflammatory regulators can become compromised. Over 600 genes have been implicated in metastasis to bone, lung or brain but how these genes might contribute to perturbation of immune function is poorly understood. To gain insight, we adopted a gene co-expression network approach that draws on the functional parallels between naturally occurring bone marrow-derived mesenchymal stem cells (BM-MSCs) and cancer stem cells (CSCs). Our network analyses indicate a key role for metastasis suppressor RARRES3, including potential to regulate the immunoproteasome (IP), a specialized proteasome induced under inflammatory conditions. Knockdown of RARRES3 in near-normal mammary epithelial and breast cancer cell lines increases overall transcript and protein levels of the IP subunits, but not of their constitutively expressed counterparts. RARRES3 mRNA expression is controlled by interferon regulatory factor IRF1, an inducer of the IP, and is sensitive to depletion of the retinoid-related receptor RORA that regulates various physiological processes including immunity through modulation of gene expression. Collectively, these findings identify a novel regulatory role for RARRES3 as an endogenous inhibitor of IP expression, and contribute to our evolving understanding of potential pathways underlying breast cancer driven immune modulation.

Indexed as

Bone Marrow CellsBreast NeoplasmsCell Line, TumorFemaleGene Expression Regulation, NeoplasticGene Regulatory NetworksHumansInterferon Regulatory Factor-1Mesenchymal Stem CellsNeoplasm MetastasisNuclear Receptor Subfamily 1, Group F, Member 1Proteasome Endopeptidase ComplexProtein SubunitsReceptors, Retinoic AcidRNA InterferenceRNA, Small InterferingInterferon Regulatory Factor-1IRF1 protein, humanNuclear Receptor Subfamily 1, Group F, Member 1PLAAT4 protein, humanProteasome Endopeptidase ComplexProtein SubunitsReceptors, Retinoic AcidRNA, Small InterferingRORA protein, human

Identifiers

PMID28051153
PMCPMC5209724
OpenAlexW2567952158

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.