Evidence map›Paper›PMID 29363717›Full record

ArticleMolecular medicine reports2018

Inhibition of microRNA-19b promotes ovarian granulosa cell proliferation by targeting IGF-1 in polycystic ovary syndrome.

Zhuohui Zhong, Fang Li, Yingying Li, Shuang Qin, Canliang Wen, Yiyuan Fu, Qing Xiao

RetractedOpen access · hybridAbstract readRetracted Publication
In one paragraph

Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 27 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 2 pooled it
7.5field-weighted citation impact, top 3% 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

27 citing papers in PubMed, 2 syntheses or guidelines pooled it, 46 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 1 country.

Zhuohui Zhong *Department of General Gynaecology, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong 510623, P.R. China.
Fang Li *Department of Obstetrics and Gynecology, Eighth People's Hospital of Guangzhou, Guangzhou, Guangdong 510060, P.R. China.
Yingying LiDepartment of General Gynaecology, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong 510623, P.R. China.
Shuang QinDepartment of General Gynaecology, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong 510623, P.R. China.
Canliang WenDepartment of General Gynaecology, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong 510623, P.R. China.
Yiyuan FuDepartment of General Gynaecology, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong 510623, P.R. China.
Qing XiaoDepartment of General Gynaecology, Guangzhou Women and Children's Medical Center, Guangzhou, Guangdong 510623, P.R. China.
Guangzhou Medical University · CNGuangzhou Women and Children Medical Center · CNGuangzhou Eighth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The purpose of the present study was to investigate the functional role of microRNA (miR)-19b in polycystic ovary syndrome (PCOS) and try to elucidate its underlying mechanisms. Expression of miR‑19b and insulin‑like growth factor 1 (IGF-1) was examined in ovarian cortexes [(from 18 women with PCOS and 10 who did not have PCOS (non‑PCOS)] and KGN cells. Cell proliferation assays (cell viability and colony formation assay) were performed following overexpression or inhibition of miR‑19b and IGF‑1 or following insulin treatment in KGN cells. Expression levels of the cell cycle-associated protein cyclin D1 and cyclin‑dependent kinase (CDK) 1 were analyzed following overexpression or inhibition of miR-19b and IGF-1. Potential miR‑19b targets were identified by bioinformatics. Luciferase assay, reverse transcription‑quantitative polymerase chain reaction and western blotting were performed to determine whether IGF‑1 was a target of miR‑19b. miR‑19b expression was significantly decreased in the PCOS ovarian cortex and KGN cells and its identified target, IGF‑1, was upregulated. miR‑19b overexpression inhibited cell proliferation at G2/M phrase. Overexpression of IGF‑1 promoted cell viability and colony formation ability in KGN cells. The expression of cyclin D1 and CDK1 was statistically increased by inhibition of miR‑19b and overexpression of IGF‑1. High concentrations of insulin decreased levels of miR‑19b, stimulated KGN cell proliferation, and elevated IGF‑1 levels. Inhibition of miR‑19b promoted ovarian granulosa cell proliferation by targeting IGF‑1 in PCOS. Insulin decreased the expression levels of miR‑19b and stimulated cell proliferation. The present study suggested that overexpression of miR‑19b may be a potential therapeutic approach for PCOS.

Indexed as

Gene Expression RegulationRNA Interference3' Untranslated RegionsCell CycleCell LineCell ProliferationCell SurvivalFemaleGranulosa CellsHumansInsulinInsulin-Like Growth Factor IMicroRNAsPolycystic Ovary Syndrome3' Untranslated RegionsInsulinInsulin-Like Growth Factor IMicroRNAsMIRN19A microRNA, humancell proliferationinsulin-like growth factor 1microRNA-19bpolycystic ovary syndrome

Identifiers

PMID29363717
PMCPMC5865948
OpenAlexW2785468279

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.