Evidence map›Paper›PMID 39905197›Full record

ArticleScientific reports2025

The impact of glucocorticoid receptor transactivation on context-dependent cell migration dynamics.

Szonja Polett Pósa, Éva Saskői, Lili Bársony, Lőrinc Pongor, Fanni Fekete, János Papp, Anikó Bozsik, Attila Patócs, Henriett Butz

Abstract read
In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. A Marine-Derived Steroid fromMarine drugs · 2025
    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

9 authors.

Szonja Polett PósaDepartment of Molecular Genetics and the National Tumor Biology Laboratory, National Institute of Oncology, Budapest, Hungary.
Éva SaskőiDepartment of Molecular Genetics and the National Tumor Biology Laboratory, National Institute of Oncology, Budapest, Hungary.
Lili BársonyDepartment of Molecular Genetics and the National Tumor Biology Laboratory, National Institute of Oncology, Budapest, Hungary.
Lőrinc PongorCancer Genomics and Epigenetics Core Group, HCEMM, Szeged, Hungary.
Fanni FeketeDepartment of Oncology Biobank, National Institute of Oncology, Budapest, Hungary.
János PappDepartment of Molecular Genetics and the National Tumor Biology Laboratory, National Institute of Oncology, Budapest, Hungary.
Anikó BozsikDepartment of Molecular Genetics and the National Tumor Biology Laboratory, National Institute of Oncology, Budapest, Hungary.
Attila PatócsDepartment of Molecular Genetics and the National Tumor Biology Laboratory, National Institute of Oncology, Budapest, Hungary.
Henriett ButzDepartment of Molecular Genetics and the National Tumor Biology Laboratory, National Institute of Oncology, Budapest, Hungary. butz.henriett@oncol.hu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The glucocorticoid receptor (GR) plays a significant role in breast cancer cell behaviour, although data on its effects are conflicting. The impact of GR agonist dexamethasone (dex) and antagonist mifepristone (mif) on oestrogen-positive (ER+) and triple-negative (TN) breast cancer cell lines in both 2D and 3D cultures was studied using multiple in vitro functional assays and transcriptome sequencing. GR activation increased cell motility in TN but not in ER + tumour cells, as observed in both collective and single-cell migration tests. Time-lapse analysis showed enhanced motility after 4-6 h in wound healing, despite dex inhibiting migration initially. This inhibition was observed at 2 h in single-cell tracking migration assays. Cell proliferation increased in TN and decreased in ER + cells upon GR activation, reversed by GR antagonist. RNA sequencing revealed dex's impact on cell adhesion and extracellular matrix signalling in TN cells and on DNA replication in ER + cells. Based on data from 1085 human breast cancer specimens, GR pathway expression correlated with migratory, extracellular matrix, and angiogenesis gene signatures. Additionally, higher expression of GR and increased GR signature were observed in fast-migrating cells compared to slow-migrating ones. Positive correlation between the GR signature and migration signature at the single-cell level indicated an association between GR activity and cell migration. For the first time, we assessed altered time-lapse migration dynamics in TN breast cancer cells, potentially contributing to cancer progression and prognosis, highlighting that the effects of dexamethasone on breast cancer cell migration are influenced by ER status and treatment duration.

Indexed as

Breast NeoplasmsCell MovementReceptors, GlucocorticoidTranscriptional ActivationCell AdhesionCell Line, TumorCell ProliferationDexamethasoneFemaleGene Expression Regulation, NeoplasticHumansMifepristoneReceptors, EstrogenTriple Negative Breast NeoplasmsDexamethasoneMifepristoneReceptors, EstrogenReceptors, GlucocorticoidBreast cancerGene expressionGlucocorticoidGlucocorticoid receptorMigrationTranscriptome

Identifiers

PMID39905197
PMCPMC11794636

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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.