Evidence map›Paper›PMID 30635567›Full record

ArticleNature communications2019

The splicing factor RBM25 controls MYC activity in acute myeloid leukemia.

Ying Ge, Mikkel Bruhn Schuster, Sachin Pundhir, Nicolas Rapin, Frederik Otzen Bagger, Nikos Sidiropoulos, Nadia Hashem, Bo Torben Porse

Abstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing 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

49 citing papers in PubMed.

  1. Article
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  4. RNF149/RBM25/MYC/PD-L1 axis promotes CD8Cellular oncology (Dordrecht, Netherlands) · 2026
    Article
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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

8 authors.

Ying GeThe Finsen Laboratory, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Ole Maaløes Vej 5, 2200, Copenhagen N, Denmark.
Mikkel Bruhn SchusterThe Finsen Laboratory, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Ole Maaløes Vej 5, 2200, Copenhagen N, Denmark.
Sachin PundhirThe Finsen Laboratory, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Ole Maaløes Vej 5, 2200, Copenhagen N, Denmark.
Nicolas RapinThe Finsen Laboratory, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Ole Maaløes Vej 5, 2200, Copenhagen N, Denmark.
Frederik Otzen BaggerThe Finsen Laboratory, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Ole Maaløes Vej 5, 2200, Copenhagen N, Denmark.
Nikos SidiropoulosThe Finsen Laboratory, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Ole Maaløes Vej 5, 2200, Copenhagen N, Denmark.
Nadia HashemThe Finsen Laboratory, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Ole Maaløes Vej 5, 2200, Copenhagen N, Denmark.
Bo Torben PorseThe Finsen Laboratory, Rigshospitalet, Faculty of Health and Medical Sciences, University of Copenhagen, Ole Maaløes Vej 5, 2200, Copenhagen N, Denmark. bo.porse@finsenlab.dk.ORCID http://orcid.org/0000-0001-6043-0844

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cancer sequencing studies have implicated regulators of pre-mRNA splicing as important disease determinants in acute myeloid leukemia (AML), but the underlying mechanisms have remained elusive. We hypothesized that "non-mutated" splicing regulators may also play a role in AML biology and therefore conducted an in vivo shRNA screen in a mouse model of CEBPA mutant AML. This has led to the identification of the splicing regulator RBM25 as a novel tumor suppressor. In multiple human leukemic cell lines, knockdown of RBM25 promotes proliferation and decreases apoptosis. Mechanistically, we show that RBM25 controls the splicing of key genes, including those encoding the apoptotic regulator BCL-X and the MYC inhibitor BIN1. This mechanism is also operative in human AML patients where low RBM25 levels are associated with high MYC activity and poor outcome. Thus, we demonstrate that RBM25 acts as a regulator of MYC activity and sensitizes cells to increased MYC levels.

Indexed as

Gene Expression Regulation, LeukemicAdaptor Proteins, Signal TransducingAnimalsCell Line, TumorFemaleHumansLeukemia, ExperimentalLeukemia, Myeloid, AcuteMiceNerve Tissue ProteinsNuclear ProteinsProto-Oncogene Proteins c-mycRNA-Binding ProteinsRNA Recognition Motif ProteinsRNA SplicingRNA Splicing FactorsAdaptor Proteins, Signal TransducingBin1 protein, mouseLUC7L3 protein, humanNerve Tissue ProteinsNuclear ProteinsProto-Oncogene Proteins c-mycRbm25 protein, mouseRNA-Binding ProteinsRNA Recognition Motif ProteinsRNA Splicing FactorsTumor Suppressor Proteins

Identifiers

PMID30635567
PMCPMC6329799

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Registered trials

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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.