Evidence map›Paper›PMID 31949550›Full record

ArticleInternational journal of clinical and experimental pathology2018

High expression of ZEB1 in endometriosis and its role in 17β-estradiol-induced epithelial-mesenchymal transition.

Rong-Feng Wu, Zong-Xiong Chen, Wei-Dong Zhou, You-Zhu Li, Zhi-Xiong Huang, Dian-Chao Lin, Lu-Lu Ren, Qing-Xi Chen, Qiong-Hua Chen

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.5field-weighted citation impact, top 16% 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

11 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Review
  3. Expression ofBiomedicines · 2025
    Article
  4. Article
  5. New concepts on the etiology of endometriosis.The journal of obstetrics and gynaecology research · 2023
    Article
  6. Article
  7. Review
  8. The Role of Long Non-Coding RNAs in Endometriosis.International journal of molecular sciences · 2021
    Review
  9. Article
  10. Review
  11. 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

9 authors at 1 institution in 1 country.

Rong-Feng WuReproductive Medical Center, The First Affiliated Hospital of Xiamen University Fujian 361003, PR China.
Zong-Xiong ChenState Key Laboratory of Cellular Stress Biology and Key Laboratory of The Ministry of Education for Coastal and Wetland Ecosystems, School of Life Sciences, Xiamen University Fujian 361102, PR China.
Wei-Dong ZhouReproductive Medical Center, The First Affiliated Hospital of Xiamen University Fujian 361003, PR China.
You-Zhu LiReproductive Medical Center, The First Affiliated Hospital of Xiamen University Fujian 361003, PR China.
Zhi-Xiong HuangState Key Laboratory of Cellular Stress Biology and Key Laboratory of The Ministry of Education for Coastal and Wetland Ecosystems, School of Life Sciences, Xiamen University Fujian 361102, PR China.
Dian-Chao LinDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University Fujian 361003, PR China.
Lu-Lu RenDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University Fujian 361003, PR China.
Qing-Xi ChenState Key Laboratory of Cellular Stress Biology and Key Laboratory of The Ministry of Education for Coastal and Wetland Ecosystems, School of Life Sciences, Xiamen University Fujian 361102, PR China.
Qiong-Hua ChenDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University Fujian 361003, PR China.
Xiamen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometriosis is an estrogen-dependent disease associated with pain and infertility. The objective of this study was to determine the expression of ZEB1 in endometriosis and its role in 17β-estradiol (E2)-induced epithelial-mesenchymal transition (EMT). 25 patients with endometriosis and 16 endometriosis-free patients were recruited for the study. Tissue expression of EMT makers was investigated by immunohistochemistry, then the expression of ZEB1 was quantified by qRT-PCR, immunohistochemistry, and western blot. The proliferation, DNA replication, and migration and invasion in ZEB1 knockdown Ishikawa cells were further respectively performed by MTS, Edu, wound healing and transwell assays. Luciferase assay was used to measure the ZEB1 promoter activity. Our results show that protein levels of E-cadherin and Keratin 18 decreased in endometriotic tissues. Meanwhile the expressions of ZEB1, Vimentin, and N-cadherin were significantly increased in endometriotic tissues. Down-regulation of ZEB1 inhibited Ishikawa cells proliferation, migration, invasion and EMT. E2 promoted the expression of ZEB1 through the ER genomic pathway, which contributed to the EMT process. The -1401 bp - -1901 bp region in the ZEB1 promoter was the main target of the E2 activity. The present results suggest that a high expression of ZEB1 plays an important role in the pathogenesis of endometriosis, and it may serve as a potential therapeutic target for endometriosis.

Indexed as

17β-estradiolEndometriosisepithelial-mesenchymal transitionZEB1

Identifiers

PMID31949550
PMCPMC6962925
OpenAlexW3006587082

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.