Evidence map›Paper›PMID 29141874›Full record

ArticleJournal of investigative medicine : the official publication of the American Federation for Clinical Research2018

S100A4 amplifies TGF-β-induced epithelial-mesenchymal transition in a pleural mesothelial cell line.

Qian Ning, Feiyan Li, Lei Wang, Hong Li, Yan Yao, Tinghua Hu, Zhongmin Sun

Open access · hybridAbstract read
In one paragraph

Article in Journal of investigative medicine : the official publication of the American Federation for Clinical Research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 17% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 20 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

7 authors at 1 institution in 1 country.

Qian NingDepartment of Respiration and Critical Care Medicine, The First Hospital Affiliated to School of Medicine of Xi'an Jiaotong University, Shaanxi, China.
Feiyan LiDepartment of Respiration and Critical Care Medicine, The First Hospital Affiliated to School of Medicine of Xi'an Jiaotong University, Shaanxi, China.
Lei WangDepartment of Respiration and Critical Care Medicine, The First Hospital Affiliated to School of Medicine of Xi'an Jiaotong University, Shaanxi, China.
Hong LiDepartment of Respiration and Critical Care Medicine, The First Hospital Affiliated to School of Medicine of Xi'an Jiaotong University, Shaanxi, China.
Yan YaoDepartment of Respiration and Critical Care Medicine, The First Hospital Affiliated to School of Medicine of Xi'an Jiaotong University, Shaanxi, China.
Tinghua HuDepartment of Respiration and Critical Care Medicine, The First Hospital Affiliated to School of Medicine of Xi'an Jiaotong University, Shaanxi, China.
Zhongmin SunDepartment of Respiration and Critical Care Medicine, The First Hospital Affiliated to School of Medicine of Xi'an Jiaotong University, Shaanxi, China.
First Affiliated Hospital of Xi'an Jiaotong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pleural fibrosis can dramatically lower the quality of life. Numerous studies have reported that epithelial-mesenchymal transition (EMT) regulated by transforming growth factor-β (TGF-β) is involved in fibrosis. However, the molecular mechanism is inadequately understood. Fibroblast-specific protein-1 (S100A4) is a target of TGF-β signaling. In our previous study, we have reported that S100A4 is highly expressed in pleural fibrosis. Thus, we suggest that S100A4 took part in the TGF-β-induced EMT in pleural fibrosis. In this study, we determined the expression of S100A4 and EMT-related markers in Met-5A cells (pleural mesothelial cells) treated with TGF-β or TGF-β inhibitor by real-time PCR and western blot. In order to explore the role of S100A4, we used siRNA to knock down the expression of S100A4 in cell model. We found that the expression of epithelial cell marker was decreased and the mesenchymal cell marker increased with S100A4 upregulation after treatment with TGF-β. Moreover, the changes of EMT-related event were restricted when the expression of S100A4 was knocked down. Conversely, S100A4 can partially rescue the EMT-related expression changes induced by TGF-β inhibitor. These findings suggest that S100A4 expression is induced by the TGF-β pathway, and silencing S100A4 expression can inhibit the process of TGF-β-induced EMT.

Indexed as

Epithelial-Mesenchymal TransitionBiomarkersCell LineCell ProliferationEpitheliumHumansPleuraPyrazolesQuinolinesS100 Calcium-Binding Protein A4Transforming Growth Factor betaBiomarkersLY-2157299PyrazolesQuinolinesS100A4 protein, humanS100 Calcium-Binding Protein A4Transforming Growth Factor betachronic diseasefibroblast growth factorsPhenotypetransforming growth factors

Identifiers

PMID29141874
PMCPMC5800353
OpenAlexW2771018860

What OpenQuestion holds

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LicenceCC BY-NC
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.