Evidence map›Paper›PMID 37735672›Full record

ArticleCell communication and signaling : CCS2023

Acute myeloid leukemia-derived exosomes deliver miR-24-3p to hinder the T-cell immune response through DENN/MADD targeting in the NF-κB signaling pathways.

Khalid Otmani, Redouane Rouas, Laurence Lagneaux, Mohammad Krayem, Hugues Duvillier, Mimoune Berehab, Philippe Lewalle

RetractedOpen access · goldAbstract readVideo-Audio MediaRetracted Publication
In one paragraph

Article in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

17 citing papers in PubMed, 32 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Khalid OtmaniExperimental Hematology Laboratory, Hematology Department, Hôpital Universitaire de Bruxelles, (H.U.B.) Institut Jules Bordet, Université Libre de Bruxelles, 90 Meylemeersch Street, 1070, Brussels, Belgium. otmani_khalid001@hotmail.com.
Redouane RouasExperimental Hematology Laboratory, Hematology Department, Hôpital Universitaire de Bruxelles, (H.U.B.) Institut Jules Bordet, Université Libre de Bruxelles, 90 Meylemeersch Street, 1070, Brussels, Belgium.
Laurence LagneauxLaboratoire de Thérapie Cellulaire Clinique (LTCC), Institut Jules Bordet, Université Libre de Bruxelles, Brussels, Belgium.
Mohammad KrayemLaboratory of Clinical and Experimental Oncology, Institut Jules Bordet, Université Libre de Bruxelles, Brussels, Belgium.
Hugues DuvillierFlow Cytometry Facility, Hôpital Universitaire de Bruxelles (H.U.B.) Institut Jules Bordet, Université Libre de Bruxelles, Brussels, Belgium.
Mimoune BerehabExperimental Hematology Laboratory, Hematology Department, Hôpital Universitaire de Bruxelles, (H.U.B.) Institut Jules Bordet, Université Libre de Bruxelles, 90 Meylemeersch Street, 1070, Brussels, Belgium.
Philippe LewalleExperimental Hematology Laboratory, Hematology Department, Hôpital Universitaire de Bruxelles, (H.U.B.) Institut Jules Bordet, Université Libre de Bruxelles, 90 Meylemeersch Street, 1070, Brussels, Belgium. Philippe.lewalle@hubruxelles.be.
Université Libre de Bruxelles · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundmicroRNAs (miRNAs) are known as potent gene expression regulators, and several studies have revealed the prognostic value of miRNAs in acute myeloid leukemia (AML) patient survival. Recently, strong evidence has indicated that miRNAs can be transported by exosomes (EXOs) from cancer cells to recipient immune microenvironment (IME) cells.

resultsWe found that AML blast-released EXOs enhance CD3 T-cell apoptosis in both CD4 and CD8 T cells. We hypothesized that miRNAs present in EXOs are key players in mediating the changes observed in AML T-cell survival. We found that miR-24-3p, a commonly overexpressed miRNA in AML, was present in released EXOs, suggesting that EXO-miR-24-3p was linked to the increased miR-24-3p levels detected in isolated AML T cells. These results were corroborated by ex vivo-generated miR-24-3p-enriched EXOs, which showed that miR-24-3p-EXOs increased apoptosis and miR-24-3p levels in T cells. We also demonstrated that overexpression of miR-24-3p increased T-cell apoptosis and affected T-cell proliferation by directly targeting DENN/MADD expression and indirectly altering the NF-κB, p-JAK/STAT, and p-ERK signaling pathways but promoting regulatory T-cell (Treg) development.

conclusionsThese results highlight a mechanism through which AML blasts indirectly impede T-cell function via transferred exosomal miR-24-3p. In conclusion, by characterizing the signaling network regulated by individual miRNAs in the leukemic IME, we aimed to discover new nonleukemic immune targets to rescue the potent antitumor function of T cells against AML blasts. Video Abstract.

Indexed as

ExosomesLeukemia, Myeloid, AcuteMicroRNAsDeath Domain Receptor Signaling Adaptor ProteinsGuanine Nucleotide Exchange FactorsHumansLymphocyte ActivationNF-kappa BSignal TransductionTumor MicroenvironmentDeath Domain Receptor Signaling Adaptor ProteinsGuanine Nucleotide Exchange FactorsMADD protein, humanMicroRNAsMIRN24 microRNA, humanNF-kappa BAMLApoptosisImmune responsemiR-24-3pT cells

Identifiers

PMID37735672
PMCPMC10515055
OpenAlexW4386928682

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.