Evidence map›Paper›PMID 29963136›Full record

ArticleOncology letters2018

Downregulation of aquaporin 3 inhibits cellular proliferation, migration and invasion in the MDA-MB-231 breast cancer cell line.

Muhammad Arif, Philip Kitchen, Matthew T Conner, Eric J Hill, David Nagel, Roslyn M Bill, Simon J Dunmore, Angel L Armesilla, Stephane Gross, Amtul R Carmichael and 2 more

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 13% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Review
  7. Aquaporin-mediated dysregulation of cell migration in disease states.Cellular and molecular life sciences : CMLS · 2023
    Review
  8. Non-Transport Functions of Aquaporins.Advances in experimental medicine and biology · 2023
    Article
  9. Clinical value and molecular mechanism of AQGPs in different tumors.Medical oncology (Northwood, London, England) · 2022
    Review
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. RSC advances · 2020
    Article
  20. 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

12 authors at 3 institutions in 1 country.

Muhammad ArifSchool of Life and Health Science, Aston University, Birmingham B4 7ET, UK.
Philip KitchenSchool of Clinical and Experimental Medicine, University of Birmingham, Birmingham B15 2TT, UK.
Matthew T ConnerResearch Institute for Healthcare Science, University of Wolverhampton, Wolverhampton WV1 1SB, UK.
Eric J HillResearch Institute for Healthcare Science, University of Wolverhampton, Wolverhampton WV1 1SB, UK.
David NagelSchool of Life and Health Science, Aston University, Birmingham B4 7ET, UK.
Roslyn M BillSchool of Life and Health Science, Aston University, Birmingham B4 7ET, UK.
Simon J DunmoreResearch Institute for Healthcare Science, University of Wolverhampton, Wolverhampton WV1 1SB, UK.
Angel L ArmesillaCardiovascular Molecular Pharmacology Group, Research Institute in Healthcare Science, School of Pharmacy, Faculty of Science and Engineering, University of Wolverhampton, Wolverhampton WV1 1SB, UK.
Stephane GrossSchool of Life and Health Science, Aston University, Birmingham B4 7ET, UK.
Amtul R CarmichaelSchool of Life and Health Science, Aston University, Birmingham B4 7ET, UK.
Alex C ConnerSchool of Clinical and Experimental Medicine, University of Birmingham, Birmingham B15 2TT, UK.
James E BrownAston Research Centre for Healthy Ageing and Aston Medical Research Institute, School of Life and Health Sciences, Aston University, Birmingham B4 7ET, UK.
Aston University · GBUniversity of Wolverhampton · GBUniversity of Birmingham · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Aquaporins are membrane proteins that regulate cellular water flow. Recently, aquaporins have been proposed as mediators of cancer cell biology. A subset of aquaporins, referred to as aquaglyceroporins are known to facilitate the transport of glycerol. The present study describes the effect of gene knockdown of the aquaglyceroporin AQP3 on MDA-MB-231 breast cancer cell proliferation, migration, invasion, adherence and response to the chemotherapeutic agent 5-fluorouracil. shRNA mediated AQP3 gene knockdown induced a 28% reduction in cellular proliferation (P<0.01), a 39% decrease in migration (P<0.0001), a 24% reduction in invasion (P<0.05) and a 25% increase in cell death at 100 µM 5-FU (P<0.01). Analysis of cell permeability to water and glycerol revealed that MDA-MB-231 cells with knocked down AQP3 demonstrated a modest decrease in water permeability (17%; P<0.05) but a more marked decrease in glycerol permeability (77%; P<0.001). These results suggest that AQP3 has a role in multiple aspects of breast cancer cell pathophysiology and therefore represents a novel target for therapeutic intervention.

Indexed as

AQP3aquaporinbreast cancerglycerolinvasionmigrationproliferation

Identifiers

PMID29963136
PMCPMC6019904
OpenAlexW2803257572

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.