Evidence map›Paper›PMID 41023051›Full record

ArticleScientific reports2025

Distinctive GABA A receptor subunit expression modulates cell specific EMT and functional responses in glioblastoma breast and ovarian cancer.

Maryam Khodaei, Narges Hosseinmardi, Majid Sirati-Sabet, Shamim Sahranavard, Mohammad Reza Shahmohammadi, Siamak Salami

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 5 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed, 1 pooled it
–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

5 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Review
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.

Maryam KhodaeiDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Narges HosseinmardiDepartment of Physiology, Medical School, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Majid Sirati-SabetDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Shamim SahranavardTraditional Medicine and Materia Medical Research Center, Department of Traditional Pharmacy, School of Traditional Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mohammad Reza ShahmohammadiFunctional Neurosurgery Research Center, Shohada Tajrish Comprehensive Neurosurgical Center of Excellence, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Siamak SalamiDepartment of Clinical Biochemistry, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran. salami.si@sbmu.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Given the emerging understanding of neurotransmitter involvement in cancer biology, GABA receptors have garnered attention for their diverse and sometimes controversial roles across cancer types. Hence, this study aimed to investigate the expression patterns of GABA-A receptors in glioblastoma, breast, and ovarian cancer cells and their impact on cellular responses via an agonist‒antagonist approach. Cell proliferation and cytotoxicity were assessed using MTT and AO/PI assays, respectively. GABA treatment significantly influenced proliferation, stimulating it in ovarian A2780CP cells overexpressing GABRG3 and inhibiting it in U87 glioblastoma cells, which showed increased expression of GABRR3. Furthermore, GABA reduced CD133+ and CD44+ stem-like populations in A2780CP cells and decreased the CD44+ fraction in MDA-MB231 cells, correlating with specific GABA-A receptor subunit expression. Migration assays revealed that GABA significantly reduced the motility of MDA-MB231 and MCF-7 cells, possibly through modulation of GABRR2 expression. EMT-related transcription factors and markers were evaluated using qPCR, flow cytometry, and Western blot analysis. Protein-level changes in EMT markers confirmed the transcriptional data, with GABA modulating E-cadherin and Vimentin expression in a cell-specific manner. These findings underscore the critical role of GABA-A receptor subtypes in promoting or suppressing cancer progression through context-dependent regulation of proliferation, stemness, migration, and EMT.

Indexed as

Breast NeoplasmsEpithelial-Mesenchymal TransitionGlioblastomaOvarian NeoplasmsReceptors, GABA-ACadherinsCell Line, TumorCell MovementCell ProliferationFemalegamma-Aminobutyric AcidGene Expression Regulation, NeoplasticHumansMCF-7 CellsCadherinsgamma-Aminobutyric AcidReceptors, GABA-ACancer cell-specific modulationEpithelial‒mesenchymal transitionGABA-A receptorsNeurotransmitter‒cancer interactions

Identifiers

PMID41023051
PMCPMC12480465

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.