Evidence map›Paper›PMID 33528916›Full record

ArticleJournal of cellular and molecular medicine2021

Brahma-Related Gene-1 (BRG1) promotes the malignant phenotype of glioblastoma cells.

Yinan Wang, Chuan He Yang, Andrew P Schultz, Michelle M Sims, Duane D Miller, Lawrence M Pfeffer

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

15 citing papers in PubMed, 21 citations in OpenAlex.

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  13. The SMARCA4NPJ precision oncology · 2023
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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 1 institution in 1 country.

Yinan WangDepartment of Pathology and Laboratory Medicine (College of Medicine), and the Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA.
Chuan He YangDepartment of Pathology and Laboratory Medicine (College of Medicine), and the Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA.
Andrew P SchultzDepartment of Pathology and Laboratory Medicine (College of Medicine), and the Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA.
Michelle M SimsDepartment of Pathology and Laboratory Medicine (College of Medicine), and the Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA.
Duane D MillerDepartment of Pharmaceutical Sciences (College of Pharmacy), University of Tennessee Health Science Center, Memphis, TN, USA.
Lawrence M PfefferDepartment of Pathology and Laboratory Medicine (College of Medicine), and the Center for Cancer Research, University of Tennessee Health Science Center, Memphis, TN, USA.ORCID 0000-0003-2809-1234
University of Tennessee Health Science Center · US

Funding

College of Medicine (UTHSC)Muirhead Chair Endowment at the University of Tennessee Health Science Center (UTHSC)
6 · The paper itself

Abstract

Glioblastoma multiforme (GBM) is an aggressive malignant brain tumour that is resistant to existing therapeutics. Identifying signalling pathways deregulated in GBM that can be targeted therapeutically is critical to improve the present dismal prognosis for GBM patients. In this report, we have identified that the BRG1 (Brahma-Related Gene-1) catalytic subunit of the SWI/SNF chromatin remodelling complex promotes the malignant phenotype of GBM cells. We found that BRG1 is ubiquitously expressed in tumour tissue from GBM patients, and high BRG1 expression levels are localized to specific brain tumour regions. Knockout (KO) of BRG1 by CRISPR-Cas9 gene editing had minimal effects on GBM cell proliferation, but significantly inhibited GBM cell migration and invasion. BRG1-KO also sensitized GBM cells to the anti-proliferative effects of the anti-cancer agent temozolomide (TMZ), which is used to treat GBM patients in the clinic, and selectively altered STAT3 tyrosine phosphorylation and gene expression. These results demonstrate that BRG-1 promotes invasion and migration, and decreases chemotherapy sensitivity, indicating that it functions in an oncogenic manner in GBM cells. Taken together, our findings suggest that targeting BRG1 in GBM may have therapeutic benefit in the treatment of this deadly form of brain cancer.

Indexed as

PhenotypeBiomarkers, TumorBrain NeoplasmsCell Line, TumorComputational BiologyDNA HelicasesGene EditingGene Expression ProfilingGene Expression Regulation, NeoplasticGlioblastomaHumansNuclear ProteinsTranscription FactorsTranscriptomeBiomarkers, TumorDNA HelicasesNuclear ProteinsSMARCA4 protein, humanTranscription FactorsBRG1cell migration and invasiongene expressionglioblastomaSTAT3

Identifiers

PMID33528916
PMCPMC7957270
OpenAlexW3127764475

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.