Evidence map›Paper›PMID 29116025›Full record

ArticleStem cell research & therapy2017

miR-200c suppresses endometriosis by targeting MALAT1 in vitro and in vivo.

Zongwen Liang, Yijie Chen, Yuan Zhao, Chaoyi Xu, Anqi Zhang, Qiong Zhang, Danhan Wang, Jing He, Wenfeng Hua, Ping Duan

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Stem cell research & therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
61citing papers in PubMed, 1 pooled it
11.5field-weighted citation impact, top 1% 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

61 citing papers in PubMed, 1 synthesis or guideline pooled it, 107 citations in OpenAlex.

  1. Pooled it
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  16. Linc-ROR Promotes EMT by Targeting miR-204-5p/SMAD4 in Endometriosis.Reproductive sciences (Thousand Oaks, Calif.) · 2023
    Article
  17. Article
  18. Article
  19. Article
  20. Applications of nanomaterials in endometriosis treatment.Frontiers in bioengineering and biotechnology · 2023
    Review

1 more citing papers are in PubMed but not listed here.

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

10 authors at 3 institutions in 1 country.

Zongwen LiangDepartment of Obstetrics and Gynecology, The Second Affliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, 325027, Zhejiang, China.
Yijie ChenDepartment of Obstetrics and Gynecology, The Second Affliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, 325027, Zhejiang, China.
Yuan ZhaoDepartment of Obstetrics and Gynecology, The Second Affliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, 325027, Zhejiang, China.
Chaoyi XuDepartment of Obstetrics and Gynecology, The Second Affliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, 325027, Zhejiang, China.
Anqi ZhangDepartment of Obstetrics and Gynecology, The Second Affliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, 325027, Zhejiang, China.
Qiong ZhangDepartment of Obstetrics and Gynecology, The Second Affliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, 325027, Zhejiang, China.
Danhan WangDepartment of Obstetrics and Gynecology, The Second Affliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, 325027, Zhejiang, China.
Jing HeDepartment of Pediatric Surgery, Guangzhou Institute of Pediatrics, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510623, Guangdong, China.
Wenfeng HuaDepartment of Laboratory Medicine and Central Laboratories, Guangdong Second Provincial General Hospital, Southern Medical University, Guangzhou, 510317, Guangdong, China. huawf@gd2h.org.cn.ORCID http://orcid.org/0000-0002-2300-6427
Ping DuanDepartment of Obstetrics and Gynecology, The Second Affliated Hospital and Yuying Children's Hospital, Wenzhou Medical University, Wenzhou, 325027, Zhejiang, China. dppddpp@126.com.
Wenzhou Medical University · CNGuangdong Provincial People's Hospital · CNGuangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundEndometriosis is a common, benign, and estrogen-dependent disease characterized by pelvic pain and infertility. To date, the pathogenesis of endometriosis remains unclear. Recent studies have demonstrated that noncoding RNAs, including microRNAs and long noncoding RNAs, play important roles in the development of endometriosis.

methodsExpression profiling of miRNAs in endometrial tissue was characterized using microarrays. The most differentially expressed miRNAs were confirmed using quantitative reverse transcriptase-polymerase chain reaction analysis in additional ectopic endometrial (n = 27) and normal endometrial (n = 12) tissues. For in-vitro functional studies, 5-ethynyl-2'-deoxyuridine incorporation assay, Transwell assay, and dual-luciferase reporter assay were used to measure the proliferation, migration, and luciferase activity of miR-200c and the predicted targets of miR-200c in primary endometrial stromal cells (HESCs) derived from human endometrial biopsies, respectively. For in-vivo therapeutic interventions, polymeric nanoparticles of polyethylenimine-polyethylene glycol-arginine-glycine-aspartic acid were used for delivery of miR-200c mimic and inhibitor to determine the therapeutic effect of miR-200c in a rat model of endometriosis.

resultsExogenous overexpression of miR-200c inhibited the proliferation and migration of HESCs, which were mainly regulated by metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). In contrast, inhibition of miR-200c promoted the proliferation and migration of HESCs, while the simultaneous silencing of MALAT1 expression exerted the opposite effects. We demonstrated that expression of MALAT1 in ectopic endometrial specimens was negatively correlated with that of miR-200c and that MALAT1 knockdown increased the level of miR-200c in HESCs. Moreover, the transfection of endometrial stromal cells with the miR-200c mimic or MALAT1 siRNAs decreased the protein levels of mesenchymal markers ZEB1, ZEB2, and N-cadherin and increased the protein levels of the epithelial marker E-cadherin. Furthermore, using a rat endometriosis model, we showed that local delivery of the miR-200c mimic significantly inhibited the growth of ectopic endometriotic lesions.

conclusionsThe MALAT1/miR-200c sponge may be a potential therapeutic target for endometriosis.

Indexed as

Cell Line, TumorCell ProliferationEndometriosisEpithelial-Mesenchymal TransitionFemaleHumansMicroRNAsNanoparticlesRNA, Long NoncodingTransfectionMALAT1 long non-coding RNA, humanMicroRNAsMIRN200 microRNA, humanRNA, Long NoncodingCompeting endogenous RNAEndometriosisEpithelial-to-mesenchymal transitionMALAT1miR-200cNanoparticle

Identifiers

PMID29116025
PMCPMC5678601
OpenAlexW2767225262

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.