Evidence map›Paper›PMID 35552758›Full record

ArticleMolecular medicine reports2022

Role of metformin in functional endometrial hyperplasia and polycystic ovary syndrome involves the regulation of MEG3/miR‑223/GLUT4 and SNHG20/miR‑4486/GLUT4 signaling.

Jie Liu, Yangchun Zhao, Long Chen, Ruilan Li, Yumei Ning, Xiuzhi Zhu

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.1field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 23 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

6 authors at 2 institutions in 1 country.

Jie LiuDepartment of Gynecology and Obstetrics, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310000, P.R. China.
Yangchun ZhaoDepartment of Gynecology and Obstetrics, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310000, P.R. China.
Long ChenPCR Laboratory, Department of Laboratory Medicine, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310000, P.R. China.
Ruilan LiDepartment of Gynecology and Obstetrics, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310000, P.R. China.
Yumei NingDepartment of Gynecology, Zhejiang Maternal and Child Health and Reproductive Health Center, Hangzhou, Zhejiang 310000, P.R. China.
Xiuzhi ZhuDepartment of Gynecology and Obstetrics, The Second Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou, Zhejiang 310000, P.R. China.
Zhejiang Chinese Medical University · CNHangzhou Women’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Metformin (MET) can effectively treat endometrial hyperplasia (EH), and the expression of glucose transporter type 4 insulin‑responsive (GLUT4) is closely associated with the development of EH. The present study aimed to verify the effect of MET in functional EH and polycystic ovary syndrome (PCOS). H&E staining was performed to analyze the severity of EH, and immunohistochemistry was performed to evaluate the expression of GLUT4 in the endometrium of PCOS rats. Reverse transcription‑quantitative PCR was used to calculate the expression of long non‑coding (lnc)RNA‑maternally expressed gene 3 (MEG3), lncRNA‑small nucleolar RNA host gene 20 (SNHG20), GLUT4 mRNA, microRNA (miR)‑223 and miR‑4486. Sequence analysis and luciferase assays were performed to explore the regulatory relationship among certain lncRNAs, miRNAs and target genes. EH in PCOS rats was efficiently inhibited by MET administration. The increased expression of GLUT4 in PCOS rats was attenuated by MET treatment. Moreover, the expression levels of lncRNA‑MEG3 and lncRNA‑SNHG20 were significantly inhibited in the endometrium of PCOS rats. MET treatment also showed remarkable efficiency in restoring the expression of lncRNA‑MEG3 and lncRNA‑SNHG20. Meanwhile, the expression levels of miR‑223 and miR‑4486 were notably elevated in the endometrium of PCOS rats, while MET treatment reduced the expression of miR‑223 and miR‑4486 in PCOS rats. Furthermore, a luciferase assay confirmed the inhibitory relationship between miR‑223 and lncRNA‑MEG3/GLUT4 expression, as well as between miR‑4486 and lncRNA‑SNHG20/GLUT4 expression. GLUT4 knockdown restored the decreased viability of HCC‑94 cells induced by overexpression of lncRNA‑MEG3. To conclude, MET exhibited a therapeutic effect in the treatment of EH by modulating the lncRNA‑MEG3/miR‑223/GLUT4 and lncRNA‑SNHG20/miR‑4486/GLUT4 signaling pathways. This work provides mechanistic insight into the development of EH.

Indexed as

Carcinoma, HepatocellularEndometrial HyperplasiaLiver NeoplasmsMetforminMicroRNAsPolycystic Ovary SyndromeRNA, Long NoncodingAnimalsEndometriumFemaleGlucose Transporter Type 4HumansRatsGlucose Transporter Type 4MetforminMicroRNAsMIR223, humanMIRN223 microRNA, ratRNA, Long Noncodingendometrial hyperplasiaglucose transporter type 4maternally expressed gene 3metforminmicroRNA‑223microRNA‑4486polycystic ovary syndromesmall nucleolar RNA host gene 20

Identifiers

PMID35552758
PMCPMC9175273
OpenAlexW4280505578

What OpenQuestion holds

Textmetadata
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.