Evidence map›Paper›PMID 34789312›Full record

ArticleJournal of ovarian research2021

Long noncoding RNA SNHG25 promotes the malignancy of endometrial cancer by sponging microRNA-497-5p and increasing FASN expression.

Yuhua He, Shuifang Xu, Yi Qi, Jinfang Tian, Fengying Xu

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 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.3field-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

22 citing papers in PubMed, 34 citations in OpenAlex.

  1. Article
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  7. Advances in MiRNAs Involved in Endometrial Carcinoma.Combinatorial chemistry & high throughput screening · 2025
    Review
  8. Article
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  10. Review
  11. Article
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  15. LncRNA SNHG25 Predicts Poor Prognosis and Promotes Progression in OsteosarcomaCombinatorial chemistry & high throughput screening · 2024
    Article
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  18. Review
  19. Article
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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

5 authors at 1 institution in 1 country.

Yuhua He *Department of Gynaecology and Obstetrics, Jinshan District Tinglin Hospital, 80 North Siping Road, Jinshan District, Shanghai, 201505, China.
Shuifang Xu *Department of Gynaecology and Obstetrics, Jinshan District Tinglin Hospital, 80 North Siping Road, Jinshan District, Shanghai, 201505, China.
Yi QiDepartment of Gynaecology and Obstetrics, Jinshan District Tinglin Hospital, 80 North Siping Road, Jinshan District, Shanghai, 201505, China.
Jinfang TianDepartment of Gynaecology and Obstetrics, Jinshan District Tinglin Hospital, 80 North Siping Road, Jinshan District, Shanghai, 201505, China.
Fengying XuDepartment of Gynaecology and Obstetrics, Jinshan District Tinglin Hospital, 80 North Siping Road, Jinshan District, Shanghai, 201505, China. xu.fengying@jsdtl-hospitalsh.cn.ORCID http://orcid.org/0000-0001-9880-8283
Jinshan Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSmall nucleolar RNA host gene 25 (SNHG25), a long noncoding RNA, has been well-studied in epithelial ovarian cancer. However, the specific functions of SNHG25 in endometrial cancer (EC) have not been studied yet. In this study, we aimed to elucidate the clinical significance of SNHG25 in EC and determine the regulatory activity of SNHG25 on the tumor-associated EC phenotype. We also thoroughly explored the molecular mechanisms underlying SNHG25 function in EC.

methodsGene expression was measured using quantitative real-time polymerase chain reaction. The detailed functions of SNHG25 in EC were examined by performing loss-of-function experiments. Moreover, the regulatory mechanisms involving SNHG25, microRNA-497-5p, and fatty acid synthase (FASN) were unveiled using the luciferase reporter assay and RNA immunoprecipitation.

resultsWe observed a high level of SNHG25 in EC using the TCGA dataset and our study cohort. Patients with a high SNHG25 level had shorter overall survival than those with a low SNHG25 level. SNHG25 deficiency resulted in tumor-repressing activities in EC cells by decreasing cell proliferation, migration, and invasion and promoting cell apoptosis. Furthermore, the function of SNHG25 depletion in impairing tumor growth in vivo was confirmed. SNHG25 sequestered miR-497-5p as a competing endogenous RNA in EC and consequently positively regulated FASN expression. Thus, the decrease in miR-497-5p or increase in FASN could neutralize the modulatory actions of SNHG25 knockdown in EC cells.

conclusionsThe depletion of SNHG25 impedes the oncogenicity of EC by targeting the miR-497-5p/FASN axis. The newly elucidated SNHG25/miR-497-5p/FASN pathway may be a promising target for the molecular-targeted management of EC.

Indexed as

AnimalsApoptosisCell Line, TumorCell MovementCell ProliferationEndometrial NeoplasmsFatty Acid Synthase, Type IFemaleGene Expression Regulation, NeoplasticHumansMiceMicroRNAsRNA, Long NoncodingSurvival AnalysisXenograft Model Antitumor AssaysFASN protein, humanFatty Acid Synthase, Type IMicroRNAsMIRN497 microRNA, humanRNA, Long NoncodingceRNAEndometrial cancermiRNA spongeSNHG25

Identifiers

PMID34789312
PMCPMC8600866
OpenAlexW3211897000

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.