Evidence map›Paper›PMID 31423217›Full record

ArticleOncology letters2019

Overexpression of carbonyl reductase 1 inhibits malignant behaviors and epithelial mesenchymal transition by suppressing TGF-β signaling in uterine leiomyosarcoma cells.

Takuya Kajimura, Shun Sato, Akihiro Murakami, Maki Hayashi-Okada, Kengo Nakashima, Kotaro Sueoka, Norihiro Sugino

Open access · diamondAbstract read
In one paragraph

Article in Oncology letters, 2019. 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
1.0field-weighted citation impact, top 22% 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, 14 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.

Takuya KajimuraDepartment of Obstetrics and Gynecology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi 755-8505, Japan.
Shun SatoDepartment of Obstetrics and Gynecology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi 755-8505, Japan.
Akihiro MurakamiDepartment of Obstetrics and Gynecology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi 755-8505, Japan.
Maki Hayashi-OkadaDepartment of Obstetrics and Gynecology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi 755-8505, Japan.
Kengo NakashimaDepartment of Obstetrics and Gynecology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi 755-8505, Japan.
Kotaro SueokaDepartment of Obstetrics and Gynecology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi 755-8505, Japan.
Norihiro SuginoDepartment of Obstetrics and Gynecology, Yamaguchi University Graduate School of Medicine, Ube, Yamaguchi 755-8505, Japan.
Yamaguchi University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Carbonyl reductase 1 (CBR1) has been reported to be involved in cancer progression. Recently, we found that CBR1 overexpression inhibited malignant behaviors and the epithelial mesenchymal transition (EMT) in uterine cervical cancer. It remained unclear whether this was also the case in uterine leiomyosarcoma (uLMS), which is derived from mesenchymal cells and is a much more malignant gynecological tumor. A number of previous studies suggested that malignant behaviors are associated with EMT, even in mesenchymal malignant tumors. In the present study, we investigated whether CBR1 inhibits malignant behaviors and EMT in uLMS. We established clones of uLMS cells (SKN cells) and uterine sarcoma cells (MES-SA cells) that overexpressed CBR1. Cell proliferative, migratory and invasive activities were suppressed by CBR1 overexpression, accompanied by increases in the expressions of epithelial markers (E-cadherin and cytokeratin) and decreases in the expressions of mesenchymal markers (N-cadherin and fibronectin), suggesting that CBR1 overexpression inhibits malignant behaviors and EMT in uLMS cells. In addition, transforming growth factor-β (TGF-β) production and the subsequent signaling and phosphorylation of Smad were suppressed in the clones. To investigate the association between TGF-β and EMT, SKN cells were treated with TGF-β or a TGF-β receptor blocker (SB431542). EMT was promoted by TGF-β and inhibited by SB431542. In conclusion, this is the first study, to the best of the authors' knowledge, showing that CBR1 overexpression inhibits malignant behaviors and EMT in uLMS cells. The present study provided novel insight demonstrating that the suppressive effect of CBR1 is mediated through TGF-β signaling.

Indexed as

carbonyl reductase 1epithelial mesenchymal transitiontransforming growth factor-βuterine leiomyosarcoma

Identifiers

PMID31423217
PMCPMC6607169
OpenAlexW2947934979

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.