Evidence map›Paper›PMID 40203244›Full record

ArticleBlood advances2025

The role of miR-150-5p/E2F3/survivin axis in the pathogenesis of plasmablastic lymphoma and its therapeutic potential.

Miriam Verdú-Bou, Maria Joao Baptista, Marcelo Lima Ribeiro, Aleix Méndez-López, Núria Profitós-Pelejà, Fabian Frontzek, Gaël Roué, José Luís Mate, Mireia Pellicer, Pau Abrisqueta and 15 more

Abstract read
In one paragraph

Article in Blood advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
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

4 citing papers in PubMed.

  1. Article
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  4. 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

25 authors.

Miriam Verdú-BouDepartment of Medicine, Universitat Autònoma de Barcelona, Badalona, Spain.ORCID 0000-0003-4062-0549
Maria Joao BaptistaLymphoid Neoplasms Group, Josep Carreras Leukaemia Research Institute, Badalona, Spain.ORCID 0000-0003-3471-2535
Marcelo Lima RibeiroLymphoma Translational Group, Josep Carreras Leukaemia Research Institute, Badalona, Spain.ORCID 0000-0003-4529-7832
Aleix Méndez-LópezDepartment of Hematology, Institut Catala d'Oncologia-Germans Trias i Pujol University Hospital, Badalona, Spain.ORCID 0009-0002-0659-763X
Núria Profitós-PelejàLymphoma Translational Group, Josep Carreras Leukaemia Research Institute, Badalona, Spain.
Fabian FrontzekDepartment of Medicine A, Hematology, Oncology, and Pneumology, University Hospital Münster, Münster, Germany.
Gaël RouéLymphoma Translational Group, Josep Carreras Leukaemia Research Institute, Badalona, Spain.
José Luís MateDepartment of Pathology, Germans Trias i Pujol University Hospital, Autonomous University of Barcelona, Badalona, Spain.
Mireia PellicerLymphoma Translational Group, Josep Carreras Leukaemia Research Institute, Badalona, Spain.ORCID 0009-0007-2801-7671
Pau AbrisquetaDepartment of Hematology, Vall d'Hebron University Hospital, Barcelona, Spain.
Josep CastellvíDepartment of Pathology, Vall d'Hebron University Hospital, Barcelona, Spain.
Mariana Bastos-OreiroDepartment of Hematology, Gregorio Marañón Hospital, Madrid, Spain.ORCID 0000-0002-9431-4646
Javier MenárguezDepartment of Pathology, Gregorio Marañón Hospital, Madrid, Spain.
Miguel AlcocebaDepartment of Hematology, University Hospital of Salamanca (HUS/IBSAL), CIBERONC, Cancer Research Institute of Salamanca-IBMCC (USAL-CSIC), Salamanca, Spain.
Eva González-BarcaDepartment of Hematology, Institut Catala d'Oncologia-Duran i Reynals Hospital, Bellvitge Biomedical Research Institute, University of Barcelona, Hospitalet de Llobregat, Spain.ORCID 0000-0002-1323-1508
Fina ClimentDepartment of Pathology, Bellvitge University Hospital-IDIBELL, Hospitalet de Llobregat, Barcelona, Spain.
Antonio SalarDepartment of Hematology, Hospital del Mar, Barcelona, Spain.
Juan-Manuel SanchoLymphoid Neoplasms Group, Josep Carreras Leukaemia Research Institute, Badalona, Spain.ORCID 0000-0001-7168-6538
Annette M StaigerDepartment of Clinical Pathology, Robert Bosch Hospital, Stuttgart, Germany.ORCID 0000-0002-5896-3200
German OttDepartment of Clinical Pathology, Robert Bosch Hospital, Stuttgart, Germany.
Ioannis AnagnostopoulosDepartment of Pathology, Institute of Pathology, University of Würzburg, Würzburg, Germany.ORCID 0000-0002-5043-6043
Manel EstellerCancer Epigenetics Group, Josep Carreras Leukemia Research Institute and CIBERONC, Badalona, Spain.ORCID 0000-0003-4490-6093
Georg LenzDepartment of Medicine A, Hematology, Oncology, and Pneumology, University Hospital Münster, Münster, Germany.
Gustavo TapiaDepartment of Pathology, Germans Trias i Pujol University Hospital, Autonomous University of Barcelona, Badalona, Spain.ORCID 0000-0003-1882-0368
José-Tomás NavarroDepartment of Medicine, Universitat Autònoma de Barcelona, Badalona, Spain.ORCID 0000-0001-9101-6013

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

abstractPlasmablastic lymphoma (PBL) is an uncommon and aggressive B-cell lymphoma with a poor prognosis. Some studies have described genetic alterations in PBL, but its transcriptome has been scarcely studied, and molecular mechanisms driving lymphomagenesis remain poorly understood. Our goal was to delineate transcriptomic profiles to identify potential biomarkers for novel targeted therapy in PBL. RNA sequencing uncovered an enrichment of cell cycle-related genes, including MYC and E2F targets, and genes involved in G2/M checkpoint in PBL. Microarray analyses discovered 2 microRNA expression signatures depending on the presence of MYC translocation. Interestingly, miR-150-5p was downregulated, whereas E2F3 and BIRC5 (survivin), a cell cycle activator and an antiapoptotic regulator, respectively, were upregulated. Increasing miR-150-5p in PBL-1 cells induced G1 cell cycle arrest, suppressed proliferation by transcriptionally repressing E2F3, and promoted apoptosis by the downregulation of BIRC5. Interestingly, the miR-150-5p tumor suppressor activity was diminished in E2F3-knockdown cells. The combined inhibition of E2F3 and survivin attenuated lymphomagenesis in PBL cells and suppressed tumor growth in a chorioallantoic membrane-derived xenograft model of PBL. Overall, our study highlights the pivotal role of the miR-150-5p/E2F3/survivin axis in boosting PBL lymphomagenesis and unveils new therapeutic targets for this lymphoma.

Indexed as

E2F3 Transcription FactorMicroRNAsSurvivinAnimalsApoptosisCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansMiceBIRC5 protein, humanE2F3 protein, humanE2F3 Transcription FactorMicroRNAsMIR150, humanSurvivin

Identifiers

PMID40203244
PMCPMC12182784

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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.