Evidence map›Paper›PMID 33649815›Full record

ArticleInternational journal of molecular medicine2021

circNRIP1 facilitates keloid progression via FXR1‑mediated upregulation of miR‑503‑3p and miR‑503‑5p.

Baolin Wang, Hang Yin, Hongmei Zhang, Tiantian Wang

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

15 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Characterization of the skin keloid microenvironment.Cell communication and signaling : CCS · 2023
    Review
  6. Review
  7. CircRNAs: versatile players and new targets in organ fibrosis.Cell communication and signaling : CCS · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. 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

4 authors at 1 institution in 1 country.

Baolin WangDepartment of Dermatology, Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277100, P.R. China.
Hang YinDepartment of Neurosurgery, Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277100, P.R. China.
Hongmei ZhangDepartment of Pharmacy, Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277100, P.R. China.
Tiantian WangDepartment of Dermatology, Zaozhuang Municipal Hospital, Zaozhuang, Shandong 277100, P.R. China.
Zaozhuang Municipal Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Circular nuclear receptor interacting protein 1 (circNRIP1) is implicated in tumor initiation and progression; however, the underlying mechanism of keloid progression is unclear. To the best of our knowledge, the present study is the first to characterize the contribution of circNRIP1 to keloid progression and evaluate the potential underlying molecular mechanisms using keloid‑derived fibroblasts. The expression profile of circNRIP1 was confirmed in keloid tissue. The contribution of circNRIP1 to keloid progression was investigated via loss‑of‑function assays. Furthermore, the molecular mechanism by which circNRIP1 contributes to pre‑microRNA (miR)‑503 maturation through blocking Fbxo4‑mediated Fragile‑X mental retardation 1 (FXR1) ubiquitination was verified. Finally, the biological functions of FXR1, miR‑503‑3p, and miR‑503‑5p in keloid‑derived fibroblast proliferation, apoptosis and extracellular matrix accumulation were confirmed. circNRIP1 was highly expressed in keloid tissue and keloid‑derived fibroblasts. Functional analysis showed that circNRIP1 knockdown successfully blocked the proliferation and expression of extracellular matrix‑associated proteins while increasing the rate of apoptosis in keloid‑derived fibroblasts. Mechanistically, circNRIP1 maintained FXR1 stability by impeding Fbxo4‑mediated FXR1 ubiquitination and degradation. Additionally, FXR1 increased the abundance of miR‑503‑3p and miR‑503‑5p by contributing to pre‑miR‑503 maturation. Knockdown of FXR1, miR‑503‑3p and miR‑503‑5p also inhibited proliferation and extracellular matrix accumulation in keloid‑derived fibroblasts and increased levels of cell apoptosis. Collectively, the present study confirmed that circNRIP1 contributed to pre‑miR‑503 maturation via blocking Fbxo4‑mediated FXR1 ubiquitination and degradation, which facilitates keloid progression. These results indicate that circNRIP1 has potential as a novel therapeutic target for the control and/or treatment of keloids.

Indexed as

Cell ProliferationUp-RegulationFemaleFibroblastsHumansKeloidMaleMicroRNAsRNA-Binding ProteinsRNA, CircularFXR1 protein, humanMicroRNAsMIRN503 microRNA, humanRNA-Binding ProteinsRNA, Circularcircular nuclear receptor interacting protein 1Fragile‑X mental retardation 1keloidmicroRNA‑503‑3pmicroRNA‑503‑5p

Identifiers

PMID33649815
PMCPMC7952250
OpenAlexW3135108572

What Socratic 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 Socratic graph.