Evidence map›Paper›PMID 33630195›Full record

ArticleBreast cancer research and treatment2021

The epithelial sodium channel has a role in breast cancer cell proliferation.

Adam W Ware, Joshua J Harris, Tania L Slatter, Heather E Cunliffe, Fiona J McDonald

Abstract read
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In one paragraph

Article in Breast cancer research and treatment, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

21 citing papers in PubMed, 35 citations in OpenAlex.

  1. Strategies for Targeting Mitochondria in the Treatment of Breast Cancer.ACS pharmacology & translational science · 2026
    Review
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  11. Micronutrient Status and Breast Cancer: A Narrative Review.International journal of molecular sciences · 2024
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Ion Channel Involvement in Tumor Drug Resistance.Journal of personalized medicine · 2022
    Review
  20. International journal of general medicine · 2022
    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 1 institution in 1 country.

Adam W WareDepartment of Physiology, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand.
Joshua J HarrisDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand.
Tania L SlatterDepartment of Pathology, Dunedin School of Medicine, University of Otago, Dunedin, 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, Dunedin, New Zealand. fiona.mcdonald@otago.ac.nz.ORCID http://orcid.org/0000-0001-9242-166X
University of Otago · NZ

Funding

Lottery Health Research R-LHR-2019-101706University of Otago Research Grant ORG 0118-0319
6 · The paper itself

Abstract

purposeBreast cancer is the most common cancer affecting women worldwide with half a million associated deaths annually. Despite a huge global effort, the pathways of breast cancer progression are not fully elucidated. Ion channels have recently emerged as novel regulators of cancer cell proliferation and metastasis. The epithelial sodium channel, ENaC, made up of α, β and γ subunits is well known for its role in Na

methodsThrough the publicly available SCAN-B dataset associations between αENaC mRNA expression and breast cancer subtypes, proliferation markers and epithelial-mesenchymal transition markers (EMT) were assessed. αENaC expression, through overexpression or siRNA-mediated knockdown, and activity, through the ENaC-specific inhibitor amiloride, were altered in MCF7, T47D, BT549, and MDAMB231 breast cancer cells. MTT and EdU cell proliferation assays were used to determine the effect of these manipulations on breast cancer cell proliferation.

resultsHigh αENaC mRNA expression was associated with less aggressive and less proliferative breast cancer subtypes and with reduced expression of proliferation markers. Decreased αENaC expression or activity, in the mesenchymal breast cancer cell lines BT549 and MDAMB231, increased breast cancer cell proliferation. Conversely, increased αENaC expression decreased breast cancer cell proliferation.

conclusionαENaC expression is associated with a poor prognosis in breast cancer and is a novel regulator of breast cancer cell proliferation. Taken together, these results identify ENaC as a potential future therapeutic target.

Indexed as

Breast NeoplasmsEpithelial Sodium ChannelsCell ProliferationFemaleHumansRNA, MessengerSignal TransductionEpithelial Sodium ChannelsRNA, MessengerSCNN1A protein, humanBreast cancerEpithelial–mesenchymal transition (EMT)Epithelial sodium channel (ENaC)Proliferation

Identifiers

PMID33630195
OpenAlexW3131503652

What OpenQuestion holds

Textmetadata
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.