Evidence map›Paper›PMID 34656078›Full record

ArticleMolecular medicine (Cambridge, Mass.)2021

Human mesenchymal stem cells derived exosomes inhibit the growth of acute myeloid leukemia cells via regulating miR-23b-5p/TRIM14 pathway.

Hui Cheng, Jie Ding, Gusheng Tang, Aijie Huang, Lei Gao, Jianmin Yang, Li Chen

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular medicine (Cambridge, Mass.), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 12% 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

27 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Review
  12. Multifaceted role ofMedComm · 2024
    Review
  13. Review
  14. Article
  15. Review
  16. Review
  17. Review
  18. Review
  19. Review
  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

7 authors at 1 institution in 1 country.

Hui Cheng *Department of Hematology, Changhai, Hospital, Naval Military Medical University, Shanghai, 200433, China.ORCID 0000-0001-9154-9282
Jie Ding *Department of Hematology, Changhai, Hospital, Naval Military Medical University, Shanghai, 200433, China.
Gusheng TangDepartment of Hematology, Changhai, Hospital, Naval Military Medical University, Shanghai, 200433, China.
Aijie HuangDepartment of Hematology, Changhai, Hospital, Naval Military Medical University, Shanghai, 200433, China.
Lei GaoDepartment of Hematology, Changhai, Hospital, Naval Military Medical University, Shanghai, 200433, China.
Jianmin YangDepartment of Hematology, Changhai, Hospital, Naval Military Medical University, Shanghai, 200433, China. chyangjianmin@163.com.ORCID 0000-0002-6572-1541
Li ChenDepartment of Hematology, Changhai, Hospital, Naval Military Medical University, Shanghai, 200433, China. yuhe0628@163.com.ORCID 0000-0002-3425-4370
Second Military Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAcute myeloid leukemia (AML) is a malignancy commonly seen in adults. Previous studies indicated that TRIM14 played a tumorigenic role in various types of cancer and miR-23b-5p was down-regulated in human mesenchymal stem cell-derived exosomes (HMSC-exos) of AML patients. However, their roles in AML remains unclear. Our study aims to investigate the role of TRIM14 and miR-23b-5p in the pathogenesis of AML. MATERIALS AND

methodsThe blood specimen was collected from de novo AML patients and healthy donators. Exosomes were extracted from the culture medium of human mesenchymal stem cells under ultracentrifugation. Then exosomes were co-cultured with AML cells to determine the effect of their contents. The cell proliferation was detected by cell counting kit-8 assay, whereas the cell apoptosis was detected by flow cytometry. The expression of miR-23b-5p and TRIM14 was silenced or overexpressed to explore their biological functions in AML. Luciferase reporter assay was conducted to validate the interaction between miR-23b-5p and TRIM14. Gene expression was determined by quantitative real-time PCR and immunoblots.

resultsTRIM14 was significantly increased in AML patients and cell lines. The inhibition of TRIM14 significantly reduced the proliferation and induced the apoptosis of AML cells via activating PI3K/AKT pathway, whereas its overexpression exhibited reversed effects. HMSC-exos could suppress the proliferation of AML cells through the delivery of miR-23b-5p. Moreover, miR-23b-5p inhibited the transcription of TRIM14 by binding on its 3'UTR region. Overexpression of TRIM14 exhibited reversed effect against the function of miR-23b-5p mimic.

conclusionTRIM14 could promote the proliferation of AML cells via activating PI3K/AKT pathway, which was reversed by HMSC-exos through delivering miR-23b-5p. These findings indicated that miR-23b-5p and TRIM14 could be applied as potential targets for the treatment of AML.

Indexed as

Gene Expression Regulation, Leukemic3' Untranslated RegionsAcute DiseaseAdultApoptosisCell Line, TumorCell ProliferationCells, CulturedExosomesFemaleHL-60 CellsHumansIntracellular Signaling Peptides and ProteinsLeukemia, MyeloidMaleMesenchymal Stem Cells3' Untranslated RegionsIntracellular Signaling Peptides and ProteinsMicroRNAsMIRN23b microRNA, humanTRIM14 protein, humanTripartite Motif ProteinsAcute myeloid leukemiaExosomesHuman mesenchymal stem cellmiR-23b-5pTRIM14

Identifiers

PMID34656078
PMCPMC8520262
OpenAlexW3179366589

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.