Evidence map›Paper›PMID 31857700›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2020

S100A4/non-muscle myosin II signaling regulates epithelial-mesenchymal transition and stemness in uterine carcinosarcoma.

Masataka Tochimoto, Yasuko Oguri, Miki Hashimura, Ryo Konno, Toshihide Matsumoto, Ako Yokoi, Yoshio Kodera, Makoto Saegusa

Open access · bronzeAbstract read
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In one paragraph

Article in Laboratory investigation; a journal of technical methods and pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
3.4field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 59 citations in OpenAlex.

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  10. Uterine carcinosarcoma: Unraveling the role of epithelial-to-mesenchymal transition in progression and therapeutic potential.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Review
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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 1 institution in 1 country.

Masataka TochimotoDepartment of Pathology, Kitasato University School of Medicine, Sagamihara, Kanagawa, 252-0374, Japan.
Yasuko OguriDepartment of Pathology, Kitasato University School of Medicine, Sagamihara, Kanagawa, 252-0374, Japan.
Miki HashimuraDepartment of Pathology, Kitasato University School of Medicine, Sagamihara, Kanagawa, 252-0374, Japan.
Ryo KonnoCenter for Disease Proteomics, School of Science, Kitasato University, Sagamihara, Kanagawa, 252-0374, Japan.
Toshihide MatsumotoDepartment of Pathology, Kitasato University School of Medicine, Sagamihara, Kanagawa, 252-0374, Japan.
Ako YokoiDepartment of Pathology, Kitasato University School of Medicine, Sagamihara, Kanagawa, 252-0374, Japan.
Yoshio KoderaCenter for Disease Proteomics, School of Science, Kitasato University, Sagamihara, Kanagawa, 252-0374, Japan.
Makoto SaegusaDepartment of Pathology, Kitasato University School of Medicine, Sagamihara, Kanagawa, 252-0374, Japan. msaegusa@med.kitasato-u.ac.jp.
Kitasato University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Uterine carcinosarcoma (UCS) represents a true example of cancer associated with epithelial-mesenchymal transition (EMT), which exhibits cancer stem cell (CSC)-like traits. Although S100A4 is an inducer of EMT, little is known about its involvement in UCS tumorigenesis. Herein, we focused on the functional role of S100A4 during development of UCS. Expression of S100A4 and molecules associated with its function were also examined in 35 UCS cases. In endometrial carcinoma cell lines, S100A4 promoter activity and mRNA levels were significantly increased by the transfection of NF-κB/p65, independent of a putative κB-binding site in the promoter. Cells stably overexpressing S100A4 showed enhancement of CSC properties, along with decreased cell proliferation and acceleration of cell migration. These phenotypes were abrogated in S100A4-knockdown cells. A combination of S100A4 antibody-mediated co-immunoprecipitation and shotgun proteomics analysis revealed that S100A4 strongly interacted with non-muscle myosin II (NMII) heavy chains, including myosin 9 and myosin 14. Specific inhibition of NMII by blebbistatin phenocopied S100A4 overexpression and induced a fibroblast-like morphology. In clinical samples, S100A4 score was significantly higher in sarcomatous as compared with carcinomatous components of UCS, and was positively correlated with ALDH1, Slug, and vimentin scores, and inversely with Ki-67 labeling indices. These findings suggest that an S100A4/NMII-related signaling cascade may contribute to the establishment and maintenance of EMT/CSC properties, along with changes in cell proliferation and migration capability. These events may be initiated in carcinomatous components in UCS and lead to divergent sarcomatous differentiation.

Indexed as

S100 Calcium-Binding Protein A4CarcinosarcomaCell Line, TumorEpithelial-Mesenchymal TransitionFemaleGene Knockdown TechniquesHumansSignal TransductionUterine NeoplasmsUterusS100A4 protein, humanS100 Calcium-Binding Protein A4

Identifiers

PMID31857700
OpenAlexW2995820396

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.