Evidence map›Paper›PMID 40220219›Full record

ArticleBreast cancer research and treatment2025

Stable overexpression of the epithelial sodium channel alpha subunit reduces migration and proliferation in breast cancer cells.

Sarah R A McQueen, Wey Qi Chin, Heather E Cunliffe, Fiona J McDonald

Abstract read
In one paragraph

Article in Breast cancer research and treatment, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Sarah R A McQueenDepartment of Physiology, School of Biomedical Sciences, University of Otago, PO Box 56, Dunedin, 9054, New Zealand.
Wey Qi ChinDepartment of Physiology, School of Biomedical Sciences, University of Otago, PO Box 56, Dunedin, 9054, New Zealand.
Heather E CunliffeDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Fiona J McDonaldDepartment of Physiology, School of Biomedical Sciences, University of Otago, PO Box 56, Dunedin, 9054, New Zealand. fiona.mcdonald@otago.ac.nz.ORCID http://orcid.org/0000-0001-9242-166X

Funding

New Zealand Lottery Grants Board - Health Research R-LHR-2019-101706
6 · The paper itself

Abstract

purposeBreast cancer is the most common cancer diagnosed in women worldwide. Ion channels have emerged as novel regulators of cancer cell functions, including proliferation and migration. The epithelial sodium channel (ENaC) has a key role in blood pressure regulation, and ENaC levels affect the characteristics of several types of cancer. In breast cancer, a role for αENaC has not been investigated in migration previously nor the effect of stable overexpression of αENaC on proliferation.

methodsCorrelations of the mRNA levels for the four ENaC subunits and breast cancer survival outcomes were assessed in publicly available data and the association between αENaC and migration-related genes. Three isogenic monoclonal derivatives of MDA-MB-231 breast cancer cell lines were created with stable αENaC overexpression. Migration assays (scratch wound assay and Boyden chamber assays) and a proliferation assay (EdU) were used to determine the effect of αENaC overexpression compared to control MDA-MB-231 cells.

resultsHigher α- or δENaC expression was correlated with improved patient survival. Higher αENaC expression correlated with lower expression of migration-associated genes. Stable overexpression of αENaC in MDA-MB-231 cells resulted in reduced in vitro migration and proliferation of all three clones compared to parental control cells.

conclusionHigher αENaC expression correlates with improved patient outcomes, and overexpression in breast cancer cells reduces both cell migration and proliferation. These results highlight the possibility of ENaC as a target for future breast cancer treatments.

Indexed as

Breast NeoplasmsEpithelial Sodium ChannelsGene ExpressionCell Line, TumorCell MovementCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansPrognosisEpithelial Sodium ChannelsSCNN1A protein, humanBreast cancerEpithelial sodium channel (ENaC)MigrationProliferation

Identifiers

PMID40220219
PMCPMC12031891

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.