Evidence map›Paper›PMID 34153644›Full record

ArticleNeoplasia (New York, N.Y.)2021

Exosomal lncRNA NEAT1 from cancer-associated fibroblasts facilitates endometrial cancer progression via miR-26a/b-5p-mediated STAT3/YKL-40 signaling pathway.

Jiang-Tao Fan, Zhao-Yu Zhou, Yan-Lu Luo, Qin Luo, Si-Bang Chen, Jin-Che Zhao, Qiao-Ru Chen

Open access · goldAbstract read
In one paragraph

Article in Neoplasia (New York, N.Y.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed, 4 pooled it
6.8field-weighted citation impact, top 2% 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

59 citing papers in PubMed, 4 syntheses or guidelines pooled it, 93 citations in OpenAlex.

  1. Pooled it
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  5. Article
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  7. Phase separation and the tumor microenvironment.Cell communication and signaling : CCS · 2026
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  13. Advances in MiRNAs Involved in Endometrial Carcinoma.Combinatorial chemistry & high throughput screening · 2025
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  16. Article
  17. 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

7 authors at 1 institution in 1 country.

Jiang-Tao FanDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Province, PR China. Electronic address: fanjiangtaofjt416@163.com.
Zhao-Yu ZhouDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Province, PR China.
Yan-Lu LuoDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Province, PR China.
Qin LuoDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Province, PR China.
Si-Bang ChenDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Province, PR China.
Jin-Che ZhaoDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Province, PR China.
Qiao-Ru ChenDepartment of Obstetrics and Gynecology, The First Affiliated Hospital of Guangxi Medical University, Nanning 530021, Guangxi Province, PR China.
Guangxi Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer-associated fibroblasts cells (CAFs) confer a rapid growth and metastasis ability of endometrial cancer (EC) via exosomes-mediated cellular communication. Long non-coding RNA nuclear enriched abundant transcript 1 (lncRNA NEAT1) drives the malignant phenotypes of EC cells. However, the role of exosomal NEAT1 from CAFs in EC progression remains ambiguous, which needs to be investigated. In our study, NEAT1 and YKL-40 were up-regulated, while miR-26a/b-5p was down-regulated in EC tissues. Moreover, NEAT1 expression was increased in CAF-exosomes compared with that in NF-exosomes. In addition, the exosomal NEAT1 derived from CAFs could transfer to EC cells and promote YKL-40 expression. Further exploration showed that exosomal NEAT1 enhanced YKL-40 expression via regulating miR-26a/b-5p-STAT3 axis in EC cells. More importantly, exosomal NEAT1 accelerated in vivo tumor growth via miR-26a/b-5p-STAT3-YKL-40 axis. Taken together, our study reveals that exosomal NEAT1 from CAFs contributes to EC progression via miR-26a/b-5p-mediated STAT3/YKL-40 pathway, which indicates the therapeutic potential of exosomal NEAT1 for treating EC.

Indexed as

3' Untranslated RegionsBiomarkers, TumorCancer-Associated FibroblastsCell Line, TumorChitinase-3-Like Protein 1Coculture TechniquesEndometrial NeoplasmsExosomesFemaleGene Expression Regulation, NeoplasticHumansMicroRNAsRNA InterferenceRNA, Long NoncodingSignal TransductionSTAT3 Transcription Factor3' Untranslated RegionsBiomarkers, TumorCHI3L1 protein, humanChitinase-3-Like Protein 1MicroRNAsMIRN26 microRNA, humanNEAT1 long non-coding RNA, humanRNA, Long NoncodingSTAT3 protein, humanSTAT3 Transcription FactorCAFsECexosomemiR-26a/b-5p-STAT3-YKL-40 axisNEAT1

Identifiers

PMID34153644
PMCPMC8233173
OpenAlexW3173500988

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.