Evidence map›Paper›PMID 36293154›Full record

ArticleInternational journal of molecular sciences2022

The miR-182-5p/NDRG1 Axis Controls Endometrial Receptivity through the NF-κB/ZEB1/E-Cadherin Pathway.

Seong-Lan Yu, Yujin Kang, Da-Un Jeong, Dong Chul Lee, Hye Jin Jeon, Tae-Hyun Kim, Sung Ki Lee, Ae Ra Han, Jaeku Kang, Seok-Rae Park

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. MiR-29c-3p Impairs the Adhesion of Endometrial Epithelial Cells via COL4A1/β-catenin in Endometriosis.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026
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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

10 authors at 3 institutions in 1 country.

Seong-Lan YuPriority Research Center, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea.
Yujin KangPriority Research Center, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea.
Da-Un JeongPriority Research Center, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea.
Dong Chul LeePersonalized Genomic Medicine Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 34141, Korea.
Hye Jin JeonPriority Research Center, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea.
Tae-Hyun KimPriority Research Center, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea.
Sung Ki LeePriority Research Center, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea.
Ae Ra HanI-Dream Clinic, Department of Obstetrics and Gynecology, Mizmedi Hospital, Seoul 07639, Korea.ORCID 0000-0002-5432-548X
Jaeku KangPriority Research Center, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea.ORCID 0000-0002-8660-7940
Seok-Rae ParkPriority Research Center, Myunggok Medical Research Institute, College of Medicine, Konyang University, Daejeon 35365, Korea.ORCID 0000-0002-1407-4495
Konyang University · KRDaegu Health College · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

National Research Foundation of Korea NRF-2017R1A6A1A03015713
6 · The paper itself

Abstract

Endometrial receptivity is essential for successful pregnancy, and its impairment is a major cause of embryo-implantation failure. MicroRNAs (miRNAs) that regulate epigenetic modifications have been associated with endometrial receptivity. However, the molecular mechanisms whereby miRNAs regulate endometrial receptivity remain unclear. Therefore, we investigated whether miR-182 and its potential targets influence trophoblast cell attachment. miR-182 was expressed at lower levels in the secretory phase than in the proliferative phase of endometrium tissues from fertile donors. However, miR-182 expression was upregulated during the secretory phase in infertile women. Transfecting a synthetic miR-182-5p mimic decreased spheroid attachment of human JAr choriocarcinoma cells and E-cadherin expression (which is important for endometrial receptivity). miR-182-5p also downregulated N-Myc downstream regulated 1 (NDRG1), which was studied further. NDRG1 was upregulated in the secretory phase of the endometrium tissues and induced E-cadherin expression through the nuclear factor-κΒ (NF-κΒ)/zinc finger E-box binding homeobox 1 (ZEB1) signaling pathway. NDRG1-overexpressing or -depleted cells showed altered attachment rates of JAr spheroids. Collectively, our findings indicate that miR-182-5p-mediated NDRG1 downregulation impaired embryo implantation by upregulating the NF-κΒ/ZEB1/E-cadherin pathway. Hence, miR-182-5p is a potential biomarker for negative selection in endometrial receptivity and a therapeutic target for successful embryo implantation.

Indexed as

Infertility, FemaleMicroRNAsBiomarkersCadherinsEmbryo ImplantationEndometriumFemaleHumansNF-kappa BPregnancyZinc Finger E-box-Binding Homeobox 1BiomarkersCadherinsMicroRNAsMirn182 microRNA, humanNF-kappa BZEB1 protein, humanZinc Finger E-box-Binding Homeobox 1endometrial receptivitymiR-182-5pNDRG1NF-κΒ/ZEB1/E-cadherin pathway

Identifiers

PMID36293154
PMCPMC9602861
OpenAlexW4306385392

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.