Evidence map›Paper›PMID 34779712›Full record

ArticleCell cycle (Georgetown, Tex.)2021

miR-222-3p is involved in neural tube closure by directly targeting Ddit4 in RA induced NTDs mouse model.

Yuqing Sun, Juan Zhang, Yufei Wang, Lei Wang, Meiyan Song, Ajab Khan, Li Zhang, Bo Niu, Hong Zhao, Meining Li and 5 more

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

Article in Cell cycle (Georgetown, Tex.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.5field-weighted citation impact, top 42% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

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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

15 authors at 2 institutions in 1 country.

Yuqing SunDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth, Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, Shanxi, China.
Juan ZhangDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth, Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, Shanxi, China.
Yufei WangDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth, Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, Shanxi, China.
Lei WangDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth, Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, Shanxi, China.
Meiyan SongDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth, Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, Shanxi, China.
Ajab KhanDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth, Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, Shanxi, China.
Li ZhangDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth, Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, Shanxi, China.
Bo NiuDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth, Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, Shanxi, China.
Hong ZhaoDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth, Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, Shanxi, China.
Meining LiDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth, Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, Shanxi, China.
Tiane LuoDepartment of Statistics, Shanxi Medical University, Taiyuan, Shanxi, China.
Qiwei HeDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth, Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, Shanxi, China.
Xianghui XieMunicipal Key Laboratory of Child Development and Nutriomic, Capital Institute of Pediatrics, Beijing, China.ORCID 0000-0002-2449-8582
Zhizhen LiuDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth, Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, Shanxi, China.
Jun XieDepartment of Biochemistry and Molecular Biology, Shanxi Key Laboratory of Birth, Defect and Cell Regeneration, Shanxi Medical University, Taiyuan, Shanxi, China.
Shanxi Medical University · CNCapital Institute of Pediatrics · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previously our results showed miR-222-3p was significantly downregulated in retinoic acid-induced neural tube defect (NTD) mouse model through transcriptome. Down-regulation of miR-222-3p may be a causative biomarker in NTDs. In this study, RNA was extracted from mouse embryos at E8.5, E9.5 and E10.5, and the expression level of miR-222-3p was measured by quantitative real-time PCR analysis. The preliminary mechanism of miR-222-3p in NTDs involved in cell proliferation, apoptosis and migration was investigated in mouse HT-22 cell line. The expression of miR-222-3p was significantly decreased at E8.5, E9.5 and E10.5 developed in mouse embryos which were consistent with our transcriptome sequencing. Suppression of miR-222-3p in HT-22 cells resulted in the inhibition of cell proliferation and migration, cell cycle and apoptosis. Moreover, DNA damage transcript 4 (Ddit4) was identified as a direct and functional target of miR-222-3p. miR-222-3p is negatively regulated by Ddit4. The mutation of binding site of Ddit4 3'UTR abrogated the responsiveness of luciferase reporters to miR-222-3p and showed that Ddit4 expression partially attenuated the function of miR-222-3p. We preliminatively confirmed that low expression of miR-222-3p has reduced the expression of β-catenin, TCF4 and other related genes in the Wnt/β-catenin signaling pathway.Collectively, these results demonstrated that miR-222-3p regulates the Wnt/β-catenin signaling pathway through Ddit4 inhibition in HT-22 cells, resulted in cell proliferation and apoptosis imbalance, and thus led to neural tube defects.

Indexed as

MicroRNAsNeural Tube DefectsTranscription FactorsAnimalsbeta CateninCell Line, TumorCell MovementCell ProliferationDNA DamageGene Expression Regulation, NeoplasticMiceNeural TubeTretinoinWnt Signaling Pathwaybeta CateninDdit4 protein, mouseMicroRNAsMIRN222 microRNA, mouseTranscription FactorsTretinoinapoptosisDNA damage transcript 4 (Ddit4)miR-222-3pNeural Tube Defects (NTDS)wnt/β-catenin signaling pathway

Identifiers

PMID34779712
PMCPMC8794519
OpenAlexW3211550772

What OpenQuestion holds

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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.