Evidence map›Paper›PMID 37921359›Full record

ArticleJournal of cell science2023

The antiproliferative effect of FGF2 in K-Ras-driven tumor cells involves modulation of rRNA and the nucleolus.

Francisca N de Luna Vitorino, Michaella J Levy, Rosangela A Mansano Wailemann, Mariana Lopes, Mariana Loterio Silva, Mihaela E Sardiu, Benjamin A Garcia, Maria Cristina Machado Motta, Carla Columbano Oliveira, Hugo Aguirre Armelin and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Journal of cell science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.5field-weighted citation impact, top 32% 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

2 citing papers in PubMed, 3 citations in OpenAlex.

  1. FGF2 as a Potential Tumor Suppressor in Lung Adenocarcinoma.Diagnostics (Basel, Switzerland) · 2026
    Article
  2. Article
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

13 authors at 5 institutions in 2 countries.

Francisca N de Luna VitorinoLaboratório de Ciclo Celular - Center of Toxins, Immune-Response and Cell Signalling - CeTICS, Instituto Butantan, São Paulo, SP 055503-900, Brazil.ORCID 0000-0001-8543-2299
Michaella J LevyStowers Institute for Medical Research, Kansas City, MO 64110, USA.ORCID 0000-0003-3132-6380
Rosangela A Mansano WailemannLaboratório de Ciclo Celular - Center of Toxins, Immune-Response and Cell Signalling - CeTICS, Instituto Butantan, São Paulo, SP 055503-900, Brazil.ORCID 0000-0003-4909-9657
Mariana LopesLaboratório de Ciclo Celular - Center of Toxins, Immune-Response and Cell Signalling - CeTICS, Instituto Butantan, São Paulo, SP 055503-900, Brazil.ORCID 0000-0002-1810-9798
Mariana Loterio SilvaLaboratório de Ciclo Celular - Center of Toxins, Immune-Response and Cell Signalling - CeTICS, Instituto Butantan, São Paulo, SP 055503-900, Brazil.
Mihaela E SardiuStowers Institute for Medical Research, Kansas City, MO 64110, USA.ORCID 0000-0002-3987-7569
Benjamin A GarciaDepartment of Biochemistry and Molecular Biophysics, Washington University School of Medicine, St. Louis, MO, USA.
Maria Cristina Machado MottaLaboratório de Ultraestrutura Celular Hertha Meyer, Centro de Pesquisa em Medicina de Precisão, Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro-UFRJ, Rio de Janeiro, RJ 21491-590, Brazil.ORCID 0000-0002-0947-4830
Carla Columbano OliveiraDepartment of Biochemistry, Institute of Chemistry, University of São Paulo, São Paulo, SP 05508-000, Brazil.ORCID 0000-0002-1098-9241
Hugo Aguirre ArmelinLaboratório de Ciclo Celular - Center of Toxins, Immune-Response and Cell Signalling - CeTICS, Instituto Butantan, São Paulo, SP 055503-900, Brazil.ORCID 0000-0001-9557-0804
Laurence A FlorensStowers Institute for Medical Research, Kansas City, MO 64110, USA.ORCID 0000-0002-9310-6650
Michael P WashburnStowers Institute for Medical Research, Kansas City, MO 64110, USA.ORCID 0000-0001-7568-2585
Julia Pinheiro Chagas da CunhaLaboratório de Ciclo Celular - Center of Toxins, Immune-Response and Cell Signalling - CeTICS, Instituto Butantan, São Paulo, SP 055503-900, Brazil.ORCID 0000-0003-0466-8879
Instituto Butantan · BRStowers Institute for Medical Research · USUniversidade de São Paulo · BRUniversidade Federal do Rio de Janeiro · BRWashington University in St. Louis · US

Funding

Shared Resources Core 2: Quantitative Proteomics CoreP01CA196539 · NCI · ROCKEFELLER UNIVERSITY · PI MUIR, TOM · 2015 to 2024
$17.6M
Viral modulation of epitranscriptomic mechanismsR01AI118891 · NIAID · WASHINGTON UNIVERSITY · PI GARCIA, BENJAMIN A, WEITZMAN, MATTHEW D. · 2015 to 2025
$5.4M
Quantitative mass spectrometry for comprehending epigenetic mechanisms in a new underlying neurological developmental disorderR01HD106051 · NICHD · WASHINGTON UNIVERSITY · PI Benjamin A Garcia · 2022 to 2026
$2.6M
NCI NIH HHS P01 CA196539NIAID NIH HHS R01 AI118891NICHD NIH HHS R01 HD106051
6 · The paper itself

Abstract

The nucleolus is sensitive to stress and can orchestrate a chain of cellular events in response to stress signals. Despite being a growth factor, FGF2 has antiproliferative and tumor-suppressive functions in some cellular contexts. In this work, we investigated how the antiproliferative effect of FGF2 modulates chromatin-, nucleolus- and rDNA-associated proteins. The chromatin and nucleolar proteome indicated that FGF2 stimulation modulates proteins related to transcription, rRNA expression and chromatin-remodeling proteins. The global transcriptional rate and nucleolus area increased along with nucleolar disorganization upon 24 h of FGF2 stimulation. FGF2 stimulation induced immature rRNA accumulation by increasing rRNA transcription. The rDNA-associated protein analysis reinforced that FGF2 stimulus interferes with transcription and rRNA processing. RNA Pol I inhibition partially reversed the growth arrest induced by FGF2, indicating that changes in rRNA expression might be crucial for triggering the antiproliferative effect. Taken together, we demonstrate that the antiproliferative FGF2 stimulus triggers significant transcriptional changes and modulates the main cell transcription site, the nucleolus.

Indexed as

Cell NucleolusFibroblast Growth Factor 2ChromatinDNA, RibosomalRNA, RibosomalTranscription, GeneticChromatinDNA, RibosomalFibroblast Growth Factor 2RNA, RibosomalChromatinFGF2NucleolusProteomicsTranscription

Identifiers

PMID37921359
PMCPMC11166202
OpenAlexW4388291801

What OpenQuestion holds

Textmetadata
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.