Evidence map›Paper›PMID 37039106›Full record

ArticleThe EMBO journal2023

An ERK1/2-driven RNA-binding switch in nucleolin drives ribosome biogenesis and pancreatic tumorigenesis downstream of RAS oncogene.

Muhammad S Azman, Emilie L Alard, Martin Dodel, Federica Capraro, Rupert Faraway, Maria Dermit, Wanling Fan, Alina Chakraborty, Jernej Ule, Faraz K Mardakheh

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

22 citing papers in PubMed, 39 citations in OpenAlex.

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  9. Lysophosphatidic Acid Synergizes With 1,25-Dihydroxyvitamin D to Promote Fibroblast Growth Factor-23 Synthesis via MAPK Signaling and Induction of the IL12A Gene.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
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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

10 authors at 2 institutions in 1 country.

Muhammad S AzmanCentre for Cancer Cell and Molecular Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.
Emilie L AlardCentre for Cancer Cell and Molecular Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.
Martin DodelCentre for Cancer Cell and Molecular Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.
Federica CapraroCentre for Cancer Cell and Molecular Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0001-8974-4951
Rupert FarawayThe Francis Crick Institute, London, UK.
Maria DermitCentre for Cancer Cell and Molecular Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.
Wanling FanCentre for Cancer Cell and Molecular Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0003-0500-3350
Alina ChakrabortyCentre for Cancer Cell and Molecular Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.
Jernej UleThe Francis Crick Institute, London, UK.ORCID 0000-0002-2452-4277
Faraz K MardakhehCentre for Cancer Cell and Molecular Biology, Barts Cancer Institute, Queen Mary University of London, London, UK.ORCID 0000-0003-3896-0827
Queen Mary University of London · GBKing's College London · GB

Funding

Medical Research Council MR/P009417/1
6 · The paper itself

Abstract

Oncogenic RAS signaling reprograms gene expression through both transcriptional and post-transcriptional mechanisms. While transcriptional regulation downstream of RAS is relatively well characterized, how RAS post-transcriptionally modulates gene expression to promote malignancy remains largely unclear. Using quantitative RNA interactome capture analysis, we here reveal that oncogenic RAS signaling reshapes the RNA-bound proteomic landscape of pancreatic cancer cells, with a network of nuclear proteins centered around nucleolin displaying enhanced RNA-binding activity. We show that nucleolin is phosphorylated downstream of RAS, which increases its binding to pre-ribosomal RNA (rRNA), boosts rRNA production, and promotes ribosome biogenesis. This nucleolin-dependent enhancement of ribosome biogenesis is crucial for RAS-induced pancreatic cancer cell proliferation and can be targeted therapeutically to inhibit tumor growth. Our results reveal that oncogenic RAS signaling drives ribosome biogenesis by regulating the RNA-binding activity of nucleolin and highlight a crucial role for this mechanism in RAS-mediated tumorigenesis.

Indexed as

Genes, rasPancreatic NeoplasmsCell Transformation, NeoplasticHumansMAP Kinase Signaling SystemNucleolinPhosphoproteinsProteomicsRibosomesRNARNA, RibosomalNucleolinPhosphoproteinsRNARNA, RibosomalNucleolinpancreatic ductal adenocarcinomaRASribosome biogenesisRNA-binding proteins

Identifiers

PMID37039106
PMCPMC10233377
OpenAlexW4364352571

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.