Evidence map›Paper›PMID 32725958›Full record

ArticleJournal of cellular and molecular medicine2020

RhoA/ROCK pathway mediates the effect of oestrogen on regulating epithelial-mesenchymal transition and proliferation in endometriosis.

Zhi-Xiong Huang, Xiao-Mei Mao, Rong-Feng Wu, Shao-Min Huang, Xin-Yu Ding, Qiong-Hua Chen, Qing-Xi Chen

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
–field-weighted citation impact
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

21 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Functions of RhoA in the female reproductive system.Reproductive and developmental medicine · 2025
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

7 authors.

Zhi-Xiong HuangSchool of Life Sciences, Xiamen University, Xiamen, China.
Xiao-Mei MaoSchool of Life Sciences, Xiamen University, Xiamen, China.
Rong-Feng WuReproductive Medical Center, The First Affiliated Hospital of Xiamen University, Xiamen, China.
Shao-Min HuangReproductive Medical Center, The First Affiliated Hospital of Xiamen University, Xiamen, China.
Xin-Yu DingThe Key Laboratory of Research and Diagnosis of Gynecological Diseases of Xiamen City and Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University, Xiamen, China.
Qiong-Hua ChenThe Key Laboratory of Research and Diagnosis of Gynecological Diseases of Xiamen City and Department of Obstetrics and Gynecology, The First Affiliated Hospital of Xiamen University, Xiamen, China.
Qing-Xi ChenSchool of Life Sciences, Xiamen University, Xiamen, China.ORCID 0000-0003-4637-9813

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometriosis is a benign gynaecological disease appearing with pelvic pain, rising dysmenorrhoea and infertility seriously impacting on 10% of reproductive-age females. This research attempts to demonstrate the function and molecular mechanism of RhoA/ROCK pathway on epithelial-mesenchymal transition (EMT) and proliferation in endometriosis. The expression of Rho family was abnormally changed in endometriotic lesions; in particular, RhoA and ROCK1/2 were significantly elevated. Overexpression of RhoA in human eutopic endometrial epithelial cells (eutopic EECs) enhanced the cell mobility, epithelial-mesenchymal transition (EMT) and proliferation, and RhoA knockdown exhibited the opposite function. Oestrogen up-regulated the RhoA activity and expression of RhoA and ROCK1/2. RhoA overexpression reinforced the effect of oestrogen on promoting EMT and proliferation, and RhoA knockdown impaired the effect of oestrogen. oestrogen receptor α (ERα) was involved with the regulation of oestrogen on EMT and proliferation and up-regulated RhoA activity and expression of RhoA and ROCK1/2. The function of ERα was modulated by the change in RhoA expression. Furthermore, phosphorylated ERK that was enhanced by oestrogen and ERα promoted the protein expression of RhoA/ROCK pathway. Endometriosis mouse model revealed that oestrogen enhanced the size and weight of endometriotic lesions. The expression of RhoA and phosphorylated ERK in mouse endometriotic lesions was significantly elevated by oestrogen. We conclude that abnormal activated RhoA/ROCK pathway in endometriosis is responsible for the function of oestrogen/ERα/ERK signalling, which promoted EMT and proliferation and resulted in the development of endometriosis.

Indexed as

AdultAnimalsCells, CulturedDisease Models, AnimalEndometriosisEndometriumEpithelial-Mesenchymal TransitionEstradiolEstrogen Receptor alphaEstrogensFemaleGene Expression RegulationHumansMiceMice, Inbred BALB COvarian CystsESR1 protein, humanEstradiolEstrogen Receptor alphaEstrogensRecombinant ProteinsrhoA GTP-Binding ProteinRHOA protein, humanRhoA protein, mouserho-Associated KinasesRNA, MessengerRNA, Small InterferingROCK1 protein, humanRock1 protein, mouseROCK2 protein, humanRock2 protein, mouseendometriosisepithelial-mesenchymal transitionERKoestrogenoestrogen receptor αproliferationRhoA/ROCK pathway

Identifiers

PMID32725958
PMCPMC7521234

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.