Evidence map›Paper›PMID 27498552›Full record

ArticleMolecules and cells2016

MicroRNA-27a Inhibits Cell Migration and Invasion of Fibroblast-Like Synoviocytes by Targeting Follistatin-Like Protein 1 in Rheumatoid Arthritis.

Dong-Liang Shi, Gui-Rong Shi, Jing Xie, Xu-Zhao Du, Hao Yang

Registry-linked trialOpen access · diamondAbstract read
In one paragraph

Article in Molecules and cells, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT06290453 (The Regulatory Role of miRNA 27 and Follistatin Like Protein-1 Gene in the Pathophysiology of Multiple Sclerosis Patients.), which is not on this map. Cited by 53 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 5% 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.

NCT06290453 unknown statusnot on this mapstarted 2024, after this paper: background citation

The Regulatory Role of miRNA 27 and Follistatin Like Protein-1 Gene in the Pathophysiology of Multiple Sclerosis Patients.

TypeobservationalSponsorAssiut UniversityRan2024 to 2026Enrolled60ConditionsMultiple SclerosisArmsmicro RNA 27- FLP1 gene expression, The Expanded Disability Status Scale (EDSS), Electrophysiological assessment:, MRI examination MRI brain:
3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 1 synthesis or guideline pooled it, 94 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. microRNAs as Biomarkers and Therapeutic Targets in Rheumatoid Arthritis.International journal of molecular sciences · 2025
    Review
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Rheumatoid Arthritis and Reactive Oxygen Species: A Review.Current issues in molecular biology · 2023
    Article
  14. Review
  15. Role of follistatin-like protein 1 in liver diseases.Experimental biology and medicine (Maywood, N.J.) · 2023
    Review
  16. Review
  17. Review
  18. Organokines in Rheumatoid Arthritis: A Critical Review.International journal of molecular sciences · 2022
    Review
  19. Article
  20. Review
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.

Dong-Liang ShiNo. 1 Department of Osteopathy, Henan Province Hospital of TCM, Zhengzhou, Henan, 450002, China.
Gui-Rong ShiShangqiu Medical College, Shangqiu, Henan, 456000, China.
Jing XieNo. 1 Department of Osteopathy, Henan Province Hospital of TCM, Zhengzhou, Henan, 450002, China.
Xu-Zhao DuNo. 1 Department of Osteopathy, Henan Province Hospital of TCM, Zhengzhou, Henan, 450002, China.
Hao YangNo. 1 Department of Osteopathy, Henan Province Hospital of TCM, Zhengzhou, Henan, 450002, China.
First Affiliated Hospital of Henan University of Traditional Chinese Medicine · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibroblast-like synoviocytes (FLS) with aberrant expression of microRNA (miRNA) are critical pathogenic regulators in rheumatoid arthritis (RA). Previous studies have found that overexpression or silencing of miRNA can contribute to the development of miRNA-based therapeutics in arthritis models. In this study, we explored the effects of miR-27a on cell migration and invasion in cultured FLS from RA patients. We found that miR-27a was markedly downregulated in the serum, synovial tissue, and FLS of RA patients. Meanwhile, the expression of follistatin-like protein 1 (FSTL1) was upregulated, which suggests that FSTL1 plays a key role in RA development. The results of a Transwell assay showed that miR-27a inhibited FLS migration and invasion. However, miR-27a inhibition promoted the migration and invasion of FLS. In addition, the down-regulated expression of matrix metalloproteinases (MMP2, MMP9, and MMP13) and Rho family proteins (Rac1, Cdc42, and RhoA) was detected after treatment with miR-27a in RA-FLS by quantitative reverse transcription-PCR and western blot analysis. Then, a luciferase reporter assay validated that miR-27a targeted the 3-untranslated region (3'-UTR) of FSTL1. Moreover, miR-27a caused a significant decrease of FSTL1. In addition, the expression of TLR4 and NFκB was inhibited by miR-27a but increased by FSTL1 overexpression. In conclusion, we found that miR-27a inhibited cell migration and invasion of RA-FLS by targeting FSTL1 and restraining the TLR4/NFκB pathway.

Indexed as

AdultAgedArthritis, RheumatoidCell MovementCells, CulturedFemaleFibroblastsFollistatin-Related ProteinsGenetic TherapyHumansMaleMatrix MetalloproteinasesMicroRNAsMiddle AgedNF-kappa Brho GTP-Binding ProteinsFollistatin-Related ProteinsMatrix MetalloproteinasesMicroRNAsMIRN27 microRNA, humanNF-kappa Brho GTP-Binding ProteinsTLR4 protein, humanToll-Like Receptor 4fibroblast-like synoviocytefollistatin-like protein 1microRNArheumatoid arthritis

Identifiers

PMID27498552
PMCPMC4990753
OpenAlexW2511892904

What OpenQuestion holds

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Registered trials

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.