Evidence map›Paper›PMID 27211549›Full record

ArticleEBioMedicine2016

The Nuclear Receptor, RORγ, Regulates Pathways Necessary for Breast Cancer Metastasis.

Tae Gyu Oh, Shu-Ching M Wang, Bipul R Acharya, Joel M Goode, J Dinny Graham, Christine L Clarke, Alpha S Yap, George E O Muscat

Open access · goldAbstract read
In one paragraph

Article in EBioMedicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.5field-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

31 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. The Circadian Modulators as Molecular Targets in Cancer-A Review.International journal of molecular sciences · 2025
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  11. Identification of RORγ as a favorable biomarker for colon cancer.The Journal of international medical research · 2021
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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

8 authors at 2 institutions in 1 country.

Tae Gyu OhInstitute for Molecular Bioscience, The University of Queensland, St. Lucia, QLD 4072, Australia.
Shu-Ching M WangInstitute for Molecular Bioscience, The University of Queensland, St. Lucia, QLD 4072, Australia.
Bipul R AcharyaInstitute for Molecular Bioscience, The University of Queensland, St. Lucia, QLD 4072, Australia.
Joel M GoodeInstitute for Molecular Bioscience, The University of Queensland, St. Lucia, QLD 4072, Australia.
J Dinny GrahamWestmead Millennium Institute, Sydney Medical School, The University of Sydney, Sydney, NSW 2006, Australia.
Christine L ClarkeWestmead Millennium Institute, Sydney Medical School, The University of Sydney, Sydney, NSW 2006, Australia.
Alpha S YapInstitute for Molecular Bioscience, The University of Queensland, St. Lucia, QLD 4072, Australia.
George E O MuscatInstitute for Molecular Bioscience, The University of Queensland, St. Lucia, QLD 4072, Australia. Electronic address: g.muscat@uq.edu.au.
University of Queensland · AUUniversity of Sydney · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have previously reported that RORγ expression was decreased in ER-ve breast cancer, and increased expression improves clinical outcomes. However, the underlying RORγ dependent mechanisms that repress breast carcinogenesis have not been elucidated. Here we report that RORγ negatively regulates the oncogenic TGF-β/EMT and mammary stem cell (MaSC) pathways, whereas RORγ positively regulates DNA-repair. We demonstrate that RORγ expression is: (i) decreased in basal-like subtype cancers, and (ii) inversely correlated with histological grade and drivers of carcinogenesis in breast cancer cohorts. Furthermore, integration of RNA-seq and ChIP-chip data reveals that RORγ regulates the expression of many genes involved in TGF-β/EMT-signaling, DNA-repair and MaSC pathways (including the non-coding RNA, LINC00511). In accordance, pharmacological studies demonstrate that an RORγ agonist suppresses breast cancer cell viability, migration, the EMT transition (microsphere outgrowth) and mammosphere-growth. In contrast, RNA-seq demonstrates an RORγ inverse agonist induces TGF-β/EMT-signaling. These findings suggest pharmacological modulation of RORγ activity may have utility in breast cancer.

Indexed as

DNA RepairBenzamidesBreast NeoplasmsCell Line, TumorCell MovementCell SurvivalEpithelial-Mesenchymal TransitionFemaleFluorocarbonsGene Expression Regulation, NeoplasticHumansMCF-7 CellsNeoplasm MetastasisNuclear Receptor Subfamily 1, Group F, Member 3PiperazinesPropanols1,1,1,3,3,3-hexafluoro-2-(2-fluoro-4'-((4-(pyridin-4-ylmethyl)piperazin-1-yl)methyl)-(1,1'-biphenyl)-4-yl)propan-2-olBenzamidesFluorocarbonsNuclear Receptor Subfamily 1, Group F, Member 3PiperazinesPropanolsRORC protein, humanSR 1078Transforming Growth Factor betaBreast cancerCarcinogenesisDNA repairEMT (epithelial–mesenchymal transition)MaSC (mammary stem cell)MetastasisNuclear receptorRNA-seqRORγ (RORC, RORgamma)StemnessTGF-β (TGF-beta)

Identifiers

PMID27211549
PMCPMC4856749
OpenAlexW2280704516

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.