Evidence map›Paper›PMID 26432349›Full record

ArticleReproduction (Cambridge, England)2015

Estradiol promotes cells invasion by activating β-catenin signaling pathway in endometriosis.

Wenqian Xiong, Ling Zhang, Lan Yu, Wei Xie, Yicun Man, Yao Xiong, Hengwei Liu, Yi Liu

Open access · hybridAbstract read
In one paragraph

Article in Reproduction (Cambridge, England), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
5.1field-weighted citation impact, top 5% 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

34 citing papers in PubMed, 69 citations in OpenAlex.

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  18. PrPInternational journal of biological sciences · 2022
    Article
  19. WEE1 promotes endometriosis via the Wnt/β-catenin signaling pathway.Reproductive biology and endocrinology : RB&E · 2021
    Article
  20. Review
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 4 institutions in 1 country.

Wenqian XiongDepartment of Obstetrics and GynecologyTongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, ChinaDepartment of Obstetrics and GynecologyUnion Hospital, Huazhong University of Science and Technology, 1277 JieFang Road, Wuhan, China.
Ling ZhangDepartment of Obstetrics and GynecologyTongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, ChinaDepartment of Obstetrics and GynecologyUnion Hospital, Huazhong University of Science and Technology, 1277 JieFang Road, Wuhan, China.
Lan YuDepartment of Obstetrics and GynecologyTongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, ChinaDepartment of Obstetrics and GynecologyUnion Hospital, Huazhong University of Science and Technology, 1277 JieFang Road, Wuhan, China.
Wei XieDepartment of Obstetrics and GynecologyTongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, ChinaDepartment of Obstetrics and GynecologyUnion Hospital, Huazhong University of Science and Technology, 1277 JieFang Road, Wuhan, China.
Yicun ManDepartment of Obstetrics and GynecologyTongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, ChinaDepartment of Obstetrics and GynecologyUnion Hospital, Huazhong University of Science and Technology, 1277 JieFang Road, Wuhan, China.
Yao XiongDepartment of Obstetrics and GynecologyTongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, ChinaDepartment of Obstetrics and GynecologyUnion Hospital, Huazhong University of Science and Technology, 1277 JieFang Road, Wuhan, China.
Hengwei LiuDepartment of Obstetrics and GynecologyTongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, ChinaDepartment of Obstetrics and GynecologyUnion Hospital, Huazhong University of Science and Technology, 1277 JieFang Road, Wuhan, China.
Yi LiuDepartment of Obstetrics and GynecologyTongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, ChinaDepartment of Obstetrics and GynecologyUnion Hospital, Huazhong University of Science and Technology, 1277 JieFang Road, Wuhan, China Department of Obstetrics and GynecologyTongji Medical College, Union Hospital, Huazhong University of Science and Technology, Wuhan 430022, ChinaDepartment of Obstetrics and GynecologyUnion Hospital, Huazhong University of Science and Technology, 1277 JieFang Road, Wuhan, China liqun94@163.com.
Huazhong University of Science and Technology · CNUnion Hospital · CNUnion Hospital · CNWuhan Union Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometriosis is an estrogen-dependent disease that involves the adhesion, invasion, and angiogenesis of endometrial tissues outside of the uterine cavity. We hypothesized that a link exists between estrogen and beta-catenin (β-catenin) signaling in the pathogenesis of endometriosis. Human endometrial stromal cells (HESCs) were separated from eutopic endometrial tissues that were obtained from patients with endometriosis. β-catenin expression and cells invasiveness ability were up-regulated by 17β-estradiol (E2) in an estrogen receptor (ESR)-dependent manner, whereas β-catenin siRNA abrogated this phenomenon. Moreover, co-immunoprecipitation and dual immunofluorescence studies confirmed ESR1, β-catenin, and lymphoid enhancer factor 1/T cell factor 3 co-localization in the nucleus in HESCs after E2 treatment. To determine the role of β-catenin signaling in the implantation of ectopic endometrium, we xenotransplanted eutopic endometrium from endometriosis patients into ovariectomized severe combined immunodeficiency mice. The implantation of the endometrium was suppressed by β-catenin siRNA. Collectively, studies regarding β-catenin signaling are critical for improving our understanding of the pathogenesis of estrogen-induced endometriosis, which can translate into the development of treatments and therapeutic strategies for endometriosis.

Indexed as

AnimalsBasic Helix-Loop-Helix Proteinsbeta CateninCell MovementCells, CulturedDisease Models, AnimalDose-Response Relationship, DrugEndometriosisEndometriumEstradiolEstrogen Receptor alphaFemaleHeterograftsHumansLymphoid Enhancer-Binding Factor 1Mice, Inbred NODBasic Helix-Loop-Helix Proteinsbeta CateninCTNNB1 protein, humanESR1 protein, humanEstradiolEstrogen Receptor alphaLEF1 protein, humanLymphoid Enhancer-Binding Factor 1TCF3 protein, human

Identifiers

PMID26432349
PMCPMC4633770
OpenAlexW2180969208

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.