Evidence map›Paper›PMID 33135363›Full record

ArticleJournal of cellular and molecular medicine2020

USP15 promotes the apoptosis of degenerative nucleus pulposus cells by suppressing the PI3K/AKT signalling pathway.

Bin Yu, Bin Shen, Zhaoyu Ba, Zhonghan Liu, Jing Yuan, Weidong Zhao, Desheng Wu

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

16 citing papers in PubMed, 23 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Tissue engineering strategies for treating intervertebral disc degeneration.Frontiers in bioengineering and biotechnology · 2025
    Review
  6. Article
  7. Deubiquitylating Enzymes in Cancer and Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
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.

Bin YuDepartment of Spine Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Bin ShenDepartment of Spine Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Zhaoyu BaDepartment of Spine Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Zhonghan LiuDepartment of Spine Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Jing YuanDepartment of Spine Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Weidong ZhaoDepartment of Spine Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Desheng WuDepartment of Spine Surgery, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.ORCID 0000-0001-9414-2330
Shanghai East Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesDegenerative disc disease is characterized by an enhanced breakdown of its existing nucleus pulposus (NP) matrix due to the dysregulation of matrix enzymes and factors. Ubiquitin-specific protease 15 (USP15) is reported to be abnormal in certain human diseases. However, its role in NP degeneration remains unclear. Therefore, we aimed to explore the function of USP15 in degenerative NP cell specimens.

methodsWe induced gene silencing and overexpression of USP15 in degenerative NP cells using RNA interference (RNAi) and a lentiviral vector, respectively. qRT-PCR and Western blotting were used to determine gene and protein expression levels. Cell apoptosis was analysed via flow cytometry. Protein interaction was examined by performing a co-immunoprecipitation assay. Furthermore, the PI3K inhibitor LY294002 and agonist IGF-1 were used to investigate the link between USP15 and AKT in NP degeneration.

resultsWe found that USP15 was up-regulated in degenerative NP cells and that its overexpression accelerated the process of apoptosis. Moreover, USP15 expression levels negatively correlated with AKT phosphorylation in degenerative NP cells. Furthermore, targeting and silencing USP15 with miR-338-3p and studying its interaction with FK506-binding protein 5 (FKBP5) revealed enhancement of FKBP5 ubiquitination, indicating that USP15 is a component of the FKBP5/AKT signalling pathway in degenerative NP cells.

conclusionsOur results show that USP15 exacerbates NP degradation by deubiquitinating and stabilizing FKBP5. This in turn results in the suppression of AKT phosphorylation in degenerative NP cells. Therefore, our study provides insights into the understanding of USP15 function as a potential molecule in the network of NP degeneration.

Indexed as

ApoptosisSignal Transduction3' Untranslated RegionsCells, CulturedGene Expression RegulationHumansImmunohistochemistryImmunophenotypingInsulin-Like Growth Factor IIntervertebral Disc DegenerationMicroRNAsNucleus PulposusPhosphatidylinositol 3-KinasesProtein BindingProto-Oncogene Proteins c-aktUbiquitin-Specific Proteases3' Untranslated RegionsInsulin-Like Growth Factor IMicroRNAsMIRN338 microRNA, humanPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktUbiquitin-Specific ProteasesUSP15 protein, humanAKTdegenerative nucleus pulposusFK506-binding protein 5miR-338-3pubiquitin-specific protease 15

Identifiers

PMID33135363
PMCPMC7754067
OpenAlexW3097139021

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.