Evidence map›Paper›PMID 33180234›Full record

ArticleBreast cancer research and treatment2021

The SWI/SNF subunit SMARCD3 regulates cell cycle progression and predicts survival outcome in ER+ breast cancer.

Romain Tropée, Bárbara de la Peña Avalos, Madeline Gough, Cameron Snell, Pascal H G Duijf, Eloïse Dray

Open access · greenAbstract read
In one paragraph

Article in Breast cancer research and treatment, 2021. 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
1.3field-weighted citation impact, top 21% 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, 26 citations in OpenAlex.

  1. SMARCD1 and Its Functional Relevance in SWI/SNF and Cancer.International journal of molecular sciences · 2026
    Review
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  11. Contextual modifiers of healthspan, lifespan, and epigenome in mice under chronic social stress.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  12. Article
  13. Advances in the role of SWI/SNF complexes in tumours.Journal of cellular and molecular medicine · 2023
    Review
  14. Article
  15. Review
  16. Review
  17. Article
  18. LncRNAInternational journal of molecular sciences · 2022
    Article
  19. Article
  20. Tribbles pseudokinase 3 (Annals of translational medicine · 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

6 authors at 3 institutions in 2 countries.

Romain TropéeIHBI, Queensland University of Technology, Brisbane, QLD, Australia.ORCID http://orcid.org/0000-0003-1898-1057
Bárbara de la Peña AvalosIHBI, Queensland University of Technology, Brisbane, QLD, Australia.ORCID http://orcid.org/0000-0001-9796-8015
Madeline GoughCancer Pathology Research Group, Mater Research Institute, The University of Queensland, Translational Research Institute, 37 Kent St, Woolloongabba, QLD, 4102, Australia.
Cameron SnellCancer Pathology Research Group, Mater Research Institute, The University of Queensland, Translational Research Institute, 37 Kent St, Woolloongabba, QLD, 4102, Australia.ORCID http://orcid.org/0000-0001-7847-3041
Pascal H G DuijfIHBI, Queensland University of Technology, Brisbane, QLD, Australia.ORCID http://orcid.org/0000-0001-8646-9843
Eloïse DrayIHBI, Queensland University of Technology, Brisbane, QLD, Australia. dray@uthscsa.edu.ORCID http://orcid.org/0000-0001-6793-9838
Translational Research Institute · AUQueensland University of Technology · AUThe University of Texas MD Anderson Cancer Center · US

Funding

TISSUE CULTURE---COREP30CA054174 · NCI · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI Lei Zheng · 1991 to 2026
$59.1M
Cancer Council Queensland 2016National Breast Cancer Foundation ECR13-04NCI NIH HHS P30 CA054174
6 · The paper itself

Abstract

purposeChromatin remodeling plays an essential role in regulating transcriptional networks and timing of gene expression. Chromatin remodelers such as SWItch/Sucrose Non-Fermentable (SWI/SNF) harbor many protein components, with the catalytic subunit providing ATPase activity to displace histones along or from the DNA molecules, and associated subunits ensuring tissue specificity and transcriptional or co-transcriptional activities. Mutations in several of the SWI/SNF subunits have been linked to cancer. Here, we investigate between SMARCD3/Baf60c expression and hormone-positive (ER+) breast cancer.

methodsThe level of SMARCD3 was detected by immunohistochemistry in breast cancer patient samples, and expression levels of SMARCD1, SMARCD2, and SMARCD3 were investigated using publicly available datasets from large cohorts of breast cancer patients. Using molecular biology and microscopy, we interrogated the cellular consequences of lower SMARCD3 expression.

resultsLower proliferation rates were observed in SMARCD3-depleted cells, which reflects a failure of the cell cycle progression and an increase in endoreplication. In the absence of SMARCD3, p21 accumulates in cells, but does not halt the cell cycle, and DNA damage accumulates and remains unrepaired.

conclusionTaken together, our data begin to explain why ER+ breast cancer patients with low-SMARCD3 expressing tumors exhibit reduced survival rates compared to patients expressing normal or higher levels of SMARCD3. SMARCD3 might act as a tumor suppressor through regulation of cell cycle checkpoints and could be a reliable and specific breast cancer prognostic biomarker.

Indexed as

Breast NeoplasmsTranscription FactorsCell CycleDNA DamageFemaleHumansSucroseSucroseTranscription FactorsBreast cancerCell cycleDNA damage repairSMARCD3

Identifiers

PMID33180234
PMCPMC8262116
OpenAlexW3105449923

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.