Evidence map›Paper›PMID 33760149›Full record

ArticleMolecular medicine reports2021

miR‑143‑3p inhibits endometriotic stromal cell proliferation and invasion by inactivating autophagy in endometriosis.

Hong Yang, Tianqi Hu, Panwei Hu, Cong Qi, Lin Qian

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

Article in Molecular medicine reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.8field-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

20 citing papers in PubMed, 31 citations in OpenAlex.

  1. Article
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  6. The role of microRNAs in pregnancies complicated by maternal diabetes.Clinical science (London, England : 1979) · 2024
    Review
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  8. Article
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  17. The regulatory roles of circular RNAsFrontiers in neurology · 2022
    Review
  18. Article
  19. Pathogenesis of Endometriosis: New Insights into Prospective Therapies.International journal of molecular sciences · 2021
    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

5 authors at 1 institution in 1 country.

Hong YangDepartment of Gynaecology, Shanghai Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China.
Tianqi HuDepartment of Gynaecology, Shanghai Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China.
Panwei HuDepartment of Gynaecology, Shanghai Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China.
Cong QiDepartment of Gynaecology, Shanghai Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China.
Lin QianDepartment of Gynaecology, Shanghai Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China.
Shanghai University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endometriosis (EM) is a multifactorial and debilitating chronic benign gynecological disease, but the pathogenesis of the disease is not completely understood. Dysregulated expression of microRNAs (miRNA/miR) is associated with the etiology of EM due to their role in regulating endometrial stromal cell proliferation and invasion. The present study aimed to identify the functions and mechanisms underlying miR‑143‑3p in EM. To explore the role of miR‑143‑3p in EM, functional miRNAs were analyzed via bioinformatics analysis. miR‑143‑3p expression levels in endometriotic stromal cells (ESCs) and normal endometrial stromal cells (NESCs) were measured via reverse transcription‑quantitative PCR. The role of miR‑143‑3p in regulating ESC proliferation and invasion was assessed by performing Cell Counting Kit‑8 and Transwell assays, respectively. miR‑143‑3p expression was significantly upregulated in ESCs compared with NESCs. Functionally, miR‑143‑3p overexpression inhibited ESC proliferation and invasion, whereas miR‑143‑3p knockdown promoted ESC proliferation and invasion. Moreover, miR‑143‑3p inhibited autophagy activation in ESCs, as indicated by decreased green puncta, which represented autophagic vacuoles, decreased microtubule associated protein 1 light chain 3α expression and increased p62 expression in the miR‑143‑4p mimic group compared with the control group. Moreover, compared with the control group, miR‑143‑3p overexpression significantly decreased the expression levels of autophagy‑related 2B (ATG2B), a newly identified target gene of miR‑143‑3p, in ESCs. ATG2B overexpression reversed miR‑143‑3p overexpression‑mediated inhibition of ESC proliferation and invasion. Collectively, the results of the present study suggested that miR‑143‑3p inhibited EM progression, thus providing a novel target for the development of therapeutic agents against EM.

Indexed as

AdultAutophagyAutophagy-Related ProteinsCell MovementCell ProliferationEndometriosisEndometriumEpithelial CellsFemaleGene Expression RegulationHumansMicroRNAsMiddle AgedStromal CellsVesicular Transport ProteinsATG2B protein, humanAutophagy-Related ProteinsMicroRNAsMIRN143 microRNA, humanVesicular Transport ProteinsATG2Bautophagyendometriosisendometriotic stromal cellsmicroRNA‑143‑3p

Identifiers

PMID33760149
PMCPMC7974257
OpenAlexW3139252064

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.