Evidence map›Paper›PMID 38632473›Full record

ArticleCommunications biology2024

Cellular geometry and epithelial-mesenchymal plasticity intersect with PIEZO1 in breast cancer cells.

Choon Leng So, Mélanie Robitaille, Francisco Sadras, Michael H McCullough, Michael J G Milevskiy, Geoffrey J Goodhill, Sarah J Roberts-Thomson, Gregory R Monteith

Open access · goldAbstract read
In one paragraph

Article in Communications biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

9 citing papers in PubMed, 9 citations in OpenAlex.

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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

8 authors at 4 institutions in 2 countries.

Choon Leng SoSchool of Pharmacy, The University of Queensland, Woolloongabba, QLD, 4102, Australia.
Mélanie RobitailleSchool of Pharmacy, The University of Queensland, Woolloongabba, QLD, 4102, Australia.
Francisco SadrasSchool of Pharmacy, The University of Queensland, Woolloongabba, QLD, 4102, Australia.
Michael H McCulloughQueensland Brain Institute and School of Mathematics and Physics, The University of Queensland, Brisbane, QLD, 4072, Australia.
Michael J G MilevskiyACRF Cancer Biology and Stem Cells Division, The Walter and Eliza Hall Institute of Medical Research, Melbourne, VIC, 3052, Australia.
Geoffrey J GoodhillQueensland Brain Institute and School of Mathematics and Physics, The University of Queensland, Brisbane, QLD, 4072, Australia.ORCID 0000-0001-9789-9355
Sarah J Roberts-ThomsonSchool of Pharmacy, The University of Queensland, Woolloongabba, QLD, 4102, Australia.ORCID 0000-0001-8202-5786
Gregory R MonteithSchool of Pharmacy, The University of Queensland, Woolloongabba, QLD, 4102, Australia. gregm@uq.edu.au.ORCID 0000-0002-4345-530X
The University of Queensland · AUAustralian National University · AUJohns Hopkins University · USThe University of Melbourne · AU

Funding

Department of Health | National Health and Medical Research Council (NHMRC) 1181922Department of Health | National Health and Medical Research Council (NHMRC) 1196855
6 · The paper itself

Abstract

Differences in shape can be a distinguishing feature between different cell types, but the shape of a cell can also be dynamic. Changes in cell shape are critical when cancer cells escape from the primary tumor and undergo major morphological changes that allow them to squeeze between endothelial cells, enter the vasculature, and metastasize to other areas of the body. A shift from rounded to spindly cellular geometry is a consequence of epithelial-mesenchymal plasticity, which is also associated with changes in gene expression, increased invasiveness, and therapeutic resistance. However, the consequences and functional impacts of cell shape changes and the mechanisms through which they occur are still poorly understood. Here, we demonstrate that altering the morphology of a cell produces a remodeling of calcium influx via the ion channel PIEZO1 and identify PIEZO1 as an inducer of features of epithelial-to-mesenchymal plasticity. Combining automated epifluorescence microscopy and a genetically encoded calcium indicator, we demonstrate that activation of the PIEZO1 force channel with the PIEZO1 agonist, YODA 1, induces features of epithelial-to-mesenchymal plasticity in breast cancer cells. These findings suggest that PIEZO1 is a critical point of convergence between shape-induced changes in cellular signaling and epithelial-mesenchymal plasticity in breast cancer cells.

Indexed as

Breast NeoplasmsEndothelial CellsIon ChannelsCalciumCell PlasticityEpithelial-Mesenchymal TransitionFemaleHumansMechanotransduction, CellularCalciumIon ChannelsPIEZO1 protein, human

Identifiers

PMID38632473
PMCPMC11024093
OpenAlexW4394881747

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.