Evidence map›Paper›PMID 31414556›Full record

ArticleThe EMBO journal2019

RASSF1A is required for the maintenance of nuclear actin levels.

Maria Chatzifrangkeskou, Dafni-Eleftheria Pefani, Michael Eyres, Iolanda Vendrell, Roman Fischer, Daniela Pankova, Eric O'Neill

Open access · hybridAbstract read
In one paragraph

Article in The EMBO journal, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.4field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 46 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Recent advances in nuclear actin research.Nucleus (Austin, Tex.) · 2025
    Review
  5. Article
  6. Review
  7. Article
  8. Nuclear Actin Polymerization Regulates Cell Epithelial-Mesenchymal Transition.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023
    Article
  9. Article
  10. Article
  11. Extracellular matrix stiffness regulates degradation of MST2 via SCFBiochimica et biophysica acta. General subjects · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Karyopherin-mediated nucleocytoplasmic transport.Nature reviews. Molecular cell biology · 2022
    Review
  16. Article
  17. Nuclear Actin Dynamics in Gene Expression, DNA Repair, and Cancer.Results and problems in cell differentiation · 2022
    Article
  18. Article
  19. Review
  20. Detection of Endogenous RASSF1A Interacting Proteins.Methods in molecular biology (Clifton, N.J.) · 2021
    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

7 authors at 2 institutions in 2 countries.

Maria ChatzifrangkeskouDepartment of Oncology, University of Oxford, Oxford, UK.ORCID 0000-0003-3703-491X
Dafni-Eleftheria PefaniDepartment of Oncology, University of Oxford, Oxford, UK.ORCID 0000-0002-1956-5111
Michael EyresDepartment of Oncology, University of Oxford, Oxford, UK.
Iolanda VendrellDepartment of Oncology, University of Oxford, Oxford, UK.
Roman FischerNuffield Department of Medicine, Target Discovery Institute, University of Oxford, Oxford, UK.
Daniela PankovaDepartment of Oncology, University of Oxford, Oxford, UK.
Eric O'NeillDepartment of Oncology, University of Oxford, Oxford, UK.ORCID 0000-0002-0060-6278
University of Oxford · GBNational and Kapodistrian University of Athens · GR

Funding

Cancer Research UK 19277Cancer Research UK A19277
6 · The paper itself

Abstract

Nuclear actin participates in many essential cellular processes including gene transcription, chromatin remodelling and mRNA processing. Actin shuttles into and out the nucleus through the action of dedicated transport receptors importin-9 and exportin-6, but how this transport is regulated remains unclear. Here, we show that RASSF1A is a novel regulator of actin nucleocytoplasmic trafficking and is required for the active maintenance of nuclear actin levels through supporting binding of exportin-6 (XPO6) to RAN GTPase. RASSF1A (Ras association domain family 1 isoform A) is a tumour suppressor gene frequently silenced by promoter hypermethylation in all major solid cancers. Specifically, we demonstrate that endogenous RASSF1A localises to the nuclear envelope (NE) and is required for nucleocytoplasmic actin transport and the concomitant regulation of myocardin-related transcription factor A (MRTF-A), a co-activator of the transcription factor serum response factor (SRF). The RASSF1A/RAN/XPO6/nuclear actin pathway is aberrant in cancer cells where RASSF1A expression is lost and correlates with reduced MRTF-A/SRF activity leading to cell adhesion defects. Taken together, we have identified a previously unknown mechanism by which the nuclear actin pool is regulated and uncovered a previously unknown link of RASSF1A and MRTF-A/SRF in tumour suppression.

Indexed as

ActinsBiological TransportBreast NeoplasmsCell Line, TumorCytoplasmDNA MethylationDown-RegulationFemaleGene Expression Regulation, NeoplasticHEK293 CellsHeLa CellsHumansKaryopherinsLiver NeoplasmsNuclear EnvelopePrognosisActinsKaryopherinsMRTFA protein, humanRASSF1 protein, humanSerum Response FactorSRF protein, humanTrans-ActivatorsTumor Suppressor ProteinsXPO6 protein, humanexportin-6MRTF-Anuclear actinnuclear envelopeRASSF1A

Identifiers

PMID31414556
PMCPMC6694222
OpenAlexW2951111953

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.