Evidence map›Paper›PMID 33743811›Full record

ArticleJournal of ovarian research2021

Silencing of lncRNA UCA1 inhibited the pathological progression in PCOS mice through the regulation of PI3K/AKT signaling pathway.

Dongyong Yang, Yanqing Wang, Yajing Zheng, Fangfang Dai, Shiyi Liu, Mengqin Yuan, Zhimin Deng, Anyu Bao, Yanxiang Cheng

Open access · goldAbstract read
In one paragraph

Article in Journal of ovarian research, 2021. 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
1.9field-weighted citation impact, top 14% 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, 29 citations in OpenAlex.

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  9. Mechanism of LncRNA Gm2044 in germ cell development.Frontiers in cell and developmental biology · 2024
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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

9 authors at 2 institutions in 1 country.

Dongyong Yang *Department of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, China.
Yanqing Wang *Department of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, China.
Yajing ZhengDepartment of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, China.
Fangfang DaiDepartment of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, China.
Shiyi LiuDepartment of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, China.
Mengqin YuanDepartment of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, China.
Zhimin DengDepartment of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, China.
Anyu BaoDepartment of Clinical Laboratoy, Renmin Hospital of Wuhan University, Wuhan, China. baoanyu2008@163.com.
Yanxiang ChengDepartment of Obstetrics and Gynecology, Renmin Hospital of Wuhan University, Wuhan, China. doctoryanxicheng@163.com.
Wuhan University · CNRenmin Hospital of Wuhan University · CN

Funding

National Key R&D Program of China 2018YFC1003200National Natural Science Foundation of China 81860276
6 · The paper itself

Abstract

backgroundPolycystic ovary syndrome (PCOS) is the most common hormonal disorder among reproductive-aged women worldwide, however, the mechanisms and progression of PCOS still unclear due to its heterogeneous nature. Using the human granulosa-like tumor cell line (KGN) and PCOS mice model, we explored the function of lncRNA UCA1 in the pathological progression of PCOS.

resultsCCK8 assay and Flow cytometry were used to do the cell cycle, apoptosis and proliferation analysis, the results showed that UCA1 knockdown in KGN cells inhibited cell proliferation by blocking cell cycle progression and promoted cell apoptosis. In the in vivo experiment, the ovary of PCOS mice was injected with lentivirus carrying sh-UCA1, the results showed that knockdown of lncRNA UCA1 attenuated the ovary structural damage, increased the number of granular cells, inhibited serum insulin and testosterone release, and reduced the pro-inflammatory cytokine production. Western blot also revealed that UCA1 knockdown in PCOS mice repressed AKT activation, inhibitor experiment demonstrated that suppression of AKT signaling pathway, inhibited the cell proliferation and promoted apoptosis.

conclusionsOur study revealed that, in vitro, UCA1 knockdown influenced the apoptosis and proliferation of KGN cells, in vivo, silencing of UCA1 regulated the ovary structural damage, serum insulin release, pro-inflammatory production, and AKT signaling pathway activation, suggesting lncRNA UCA1 plays an important role in the pathological progression of PCOS.

Indexed as

AnimalsCell ProliferationDisease Models, AnimalDisease ProgressionFemaleHumansMicePhosphatidylinositol 3-KinasesPolycystic Ovary SyndromeProto-Oncogene Proteins c-aktRNA, Long NoncodingSignal TransductionPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktRNA, Long NoncodingUCA1 RNA, humanGranulosa cellInflammationlncRNAPCOSUCA1

Identifiers

PMID33743811
PMCPMC7980617
OpenAlexW3137104632

What OpenQuestion holds

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LicenceCC BY
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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.