Evidence map›Paper›PMID 30093656›Full record

ArticleScientific reports2018

Dysregulation in Actin Cytoskeletal Organization Drives Increased Stiffness and Migratory Persistence in Polyploidal Giant Cancer Cells.

Botai Xuan, Deepraj Ghosh, Emily M Cheney, Elizabeth M Clifton, Michelle R Dawson

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

51 citing papers in PubMed, 75 citations in OpenAlex.

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  19. Cells in the Polyaneuploid Cancer Cell State are Pro-Metastatic.bioRxiv : the preprint server for biology · 2024
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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

5 authors at 1 institution in 1 country.

Botai XuanBrown University, Department of Molecular Pharmacology, Physiology, and Biotechnology, Providence, 02912, USA.
Deepraj GhoshBrown University, Department of Molecular Pharmacology, Physiology, and Biotechnology, Providence, 02912, USA.
Emily M CheneyBrown University, Department of Molecular Pharmacology, Physiology, and Biotechnology, Providence, 02912, USA.
Elizabeth M CliftonBrown University, Department of Molecular Pharmacology, Physiology, and Biotechnology, Providence, 02912, USA.
Michelle R DawsonBrown University, Department of Molecular Pharmacology, Physiology, and Biotechnology, Providence, 02912, USA. michelle_dawson@brown.edu.ORCID 0000-0002-2122-4711
Brown University · US

Funding

U.S. Department of Health & Human Services | NIH | National Institute of General Medical Sciences (NIGMS) P30 GM110750
6 · The paper itself

Abstract

Polyploidal giant cancer cells (PGCCs) have been observed by pathologists in patient tumor samples and are especially prominent in late stage, high grade disease or after chemotherapy. However, they are often overlooked due to their apparent dormancy. Recent research has shown PGCCs to be chemoresistant and express stem-like features, traits associated with disease progression and relapse. Here, we show the preferential survival of PGCCs during Paclitaxel (PTX) treatment and used multiple particle tracking analysis to probe their unique biophysical phenotype. We show that PGCCs have higher inherent cytoplasmic and nuclear stiffness in order to withstand the mechanical stress associated with their increased size and the chemical stress from PTX treatment. Inhibitor studies show the involvement of a dysregulated RhoA-Rock1 pathway and overall actin cytoskeletal network as the underlying mechanism for the altered biophysical phenotype of PGCCs. Furthermore, PGCCs exhibit a slow but persistent migratory phenotype, a trait commonly associated with metastatic dissemination and invasiveness. This work demonstrates the clinical relevance and the need to study this subpopulation, in order to devise therapeutic strategies to combat disease relapse. By highlighting the unique biophysical phenotype of PGCCs, we hope to provide unique avenues for therapeutic targeting of these cells in disease treatment.

Indexed as

Actin CytoskeletonAntineoplastic Agents, PhytogenicBiophysical PhenomenaCell Line, TumorCell MovementDrug Resistance, NeoplasmFemaleGiant CellsHumansNeoplastic Stem CellsPaclitaxelPolyploidyrhoA GTP-Binding Proteinrho-Associated KinasesSignal TransductionTriple Negative Breast NeoplasmsAntineoplastic Agents, PhytogenicPaclitaxelrhoA GTP-Binding ProteinRHOA protein, humanrho-Associated KinasesROCK1 protein, human

Identifiers

PMID30093656
PMCPMC6085392
OpenAlexW2885710012

What OpenQuestion holds

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LicenceCC BY
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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.