Evidence map›Paper›PMID 37550554›Full record

ArticleJournal, genetic engineering & biotechnology2023

Molecular characterization of breast cancer cell pools with normal or reduced ability to respond to progesterone: a study based on RNA-seq.

Mariana Bustamante Eduardo, Irene Keller, Nathalie Schuster, Stefan Aebi, Rolf Jaggi

Open access · diamondAbstract read
In one paragraph

Article in Journal, genetic engineering & biotechnology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 41% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Identification and functional analysis of Rattus norvegicus Mammary carcinoma susceptibility 1b (Mcs1b) nominated variants.Mammalian genome : official journal of the International Mammalian Genome Society · 2025
    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

5 authors at 3 institutions in 2 countries.

Mariana Bustamante EduardoDepartment for BioMedical Research, University of Bern, Bern, Switzerland. mariana.bustamante@northwestern.edu.ORCID http://orcid.org/0000-0003-3785-0714
Irene KellerDepartment for BioMedical Research, University of Bern, Bern, Switzerland.
Nathalie SchusterDepartment for BioMedical Research, University of Bern, Bern, Switzerland.
Stefan AebiDepartment of Medical Oncology, Cantonal Hospital, Lucerne, Switzerland.
Rolf JaggiDepartment for BioMedical Research, University of Bern, Bern, Switzerland.
University of Bern · CHNorthwestern University · USUniversity of Lucerne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAbout one-third of patients with estrogen receptor alpha (ERα)-positive breast cancer have tumors which are progesterone receptor (PR) negative. PR is an important prognostic factor in breast cancer. Patients with ERα-positive/PR-negative tumors have shorter disease-free and overall survival than patients with ERα-positive/PR-positive tumors. New evidence has shown that progesterone (P4) has an anti-proliferative effect in ERα-positive breast cancer cells. However, the role of PR in breast cancer is only poorly understood.

methodsWe disrupted the PR gene (PGR) in ERα-positive/PR-positive T-47D cells using the CRISPR/Cas9 system. This resulted in cell pools we termed PR-low as P4 mediated effects were inhibited or blocked compared to control T-47D cells. We analyzed the gene expression profiles of PR-low and control T-47D cells in the absence of hormone and upon treatment with P4 alone or P4 together with estradiol (E2). Differentially expressed (DE) genes between experimental groups were characterized based on RNA-seq and Gene Ontology (GO) enrichment analyses.

resultsThe overall gene expression pattern was very similar between untreated PR-low and untreated control T-47D cells. More than 6000 genes were DE in control T-47D cells upon stimulation with P4 or P4 plus E2. When PR-low pools were subjected to the same hormonal treatment, up- or downregulation was either blocked/absent or consistently lower. We identified more than 3000 genes that were DE between hormone-treated PR-low and control T-47D cells. GO analysis revealed seven significantly enriched biological processes affected by PR and associated with G protein-coupled receptor (GPCR) pathways which have been described to support growth, invasiveness, and metastasis in breast cancer cells.

conclusionsThe present study provides new insights into the complex role of PR in ERα-positive/PR-positive breast cancer cells. Many of the genes affected by PR are part of central biological processes of tumorigenesis.

Indexed as

Breast cancerCRISPR/Cas9Estrogen receptor alphaGene expressionProgesterone receptorRNA sequencing

Identifiers

PMID37550554
PMCPMC10406740
OpenAlexW4385621592

What OpenQuestion holds

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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.