Evidence map›Paper›PMID 40690373›Full record

ArticleeLife2025

A single cysteine residue in vimentin regulates long non-coding RNA

Saima Usman, William Andrew Yeudall, Muy-Teck Teh, Fatemah Ghloum, Hemanth Tummala, Ahmad Waseem

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

6 authors.

Saima UsmanCentre for Oral Immunobiology and Regenerative Medicine, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.ORCID https://orcid.org/0000-0002-2679-5628
William Andrew YeudallDepartment of Oral Biology and Diagnostic Sciences, The Dental College of Georgia, Augusta University, Augusta, United States.ORCID https://orcid.org/0000-0002-5279-6333
Muy-Teck TehCentre for Oral Immunobiology and Regenerative Medicine, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.ORCID https://orcid.org/0000-0002-7725-8355
Fatemah GhloumCentre for Oral Immunobiology and Regenerative Medicine, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.ORCID https://orcid.org/0009-0007-5775-5518
Hemanth TummalaCentre for Genomics and Child Health, Blizard Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.ORCID https://orcid.org/0000-0002-1413-745X
Ahmad WaseemCentre for Oral Immunobiology and Regenerative Medicine, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, United Kingdom.ORCID https://orcid.org/0000-0002-7941-266X

Funding

EPS8 as a Driver of the Oral Cancer Initiating Cell Phenotype.R01DE024381 · NIDCR · VIRGINIA COMMONWEALTH UNIVERSITY · PI YEUDALL, WILLIAM ANDREW · 2014 to 2017
$1.3M
NIDCR NIH HHS 5R01DE024381NIDCR NIH HHS R01 DE024381
6 · The paper itself

Abstract

Vimentin is a type III intermediate filament (IF) protein that is induced in a large number of solid tumours. A single cysteine at position 328 in vimentin plays a crucial role in assembly, organisation, and stability of IFs. However, its exact function during epithelial-mesenchymal transition (EMT) and cancer progression has not been investigated. To investigate this, we have transduced wildtype (WT) and C328S vimentin separately in MCF-7 cells that lack endogenous vimentin. The expression of C328-VIM impacted vimentin-actin interactions and induced EMT-like features that include enhanced cell proliferation, migration, and invasion accompanied by reduced cell adhesion when compared to the wildtype cells. Functional transcriptomic studies confirmed the upregulation of EMT and mesenchymal markers, downregulation of epithelial markers, as well as acquisition of signatures associated with cancer stemness (

Indexed as

Breast NeoplasmsCysteineEpithelial-Mesenchymal TransitionNeoplastic Stem CellsRNA, Long NoncodingVimentinAnimalsCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMCF-7 CellsMiceCysteineRNA, Long NoncodingVimentinVIM protein, humanXIST non-coding RNAbreast cancer signaturecancer biologycancer stem cellscell biologyhumanintermediate filamentsmetastasismouseRNA interferenceRNA-Seqviruses

Identifiers

PMID40690373
PMCPMC12279371

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.