Evidence map›Paper›PMID 19716794›Full record

ArticleMolecular cell2009

RSK is a principal effector of the RAS-ERK pathway for eliciting a coordinate promotile/invasive gene program and phenotype in epithelial cells.

Ulrik Doehn, Camilla Hauge, Scott R Frank, Claus J Jensen, Katarzyna Duda, Jakob V Nielsen, Michael S Cohen, Jens V Johansen, Benny R Winther, Leif R Lund and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 132 papers.

0numbers the graph read from it
0cells of the map it votes in
132citing papers in PubMed
8.1field-weighted citation impact, top 2% 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

132 citing papers in PubMed, 220 citations in OpenAlex.

  1. Review
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  5. Review
  6. Discovery of a novel RSK2 inhibitor for the treatment of metastatic pancreatic cancer.Journal of enzyme inhibition and medicinal chemistry · 2025
    Article
  7. Article
  8. Review
  9. Article
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  11. Review
  12. Review
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  18. Isorhamnetin exerts anti-tumor activity in DEN + CClMedical oncology (Northwood, London, England) · 2023
    Article
  19. Article
  20. Article

72 more citing papers are in PubMed but not listed here.

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

14 authors at 4 institutions in 2 countries.

Ulrik DoehnBiotech Research & Innovation Centre (BRIC) and Centre for Epigenetics, University of Copenhagen, 2200 Copenhagen N, Denmark.
Camilla Hauge
Scott R Frank
Claus J Jensen
Katarzyna Duda
Jakob V Nielsen
Michael S Cohen
Jens V Johansen
Benny R Winther
Leif R Lund
Ole Winther
Jack Taunton
Steen H Hansen
Morten Frödin
University of Copenhagen · DKBoston Children's Hospital · USHoward Hughes Medical Institute · USGlostrup Hospital · DK

Funding

Rnd Effector Molecules in Epithelial Cell TransformationR01CA092354 · NCI · BOSTON CHILDREN'S HOSPITAL · PI HANSEN, STEEN HENNING · 2003 to 2007
$2.2M
Highly Selective, Irreversible Protein Kinase InhibitorsR01GM071434 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TAUNTON, JACK · 2005 to 2008
$1.1M
ACL HHS U18DP006133NCCDPHP CDC HHS U18 DP006133NCI NIH HHS R01 CA092354NIGMS NIH HHS R01 GM071434NIGMS NIH HHS R01 GM71434
6 · The paper itself

Abstract

The RAS-stimulated RAF-MEK-ERK pathway confers epithelial cells with critical motile and invasive capacities during development, tissue regeneration, and carcinoma progression, often via promoting the epithelial-mesenchymal transition (EMT). Many mechanisms by which ERK exerts this control remain elusive. We demonstrate that the ERK-activated kinase RSK is necessary to induce mesenchymal motility and invasive capacities in nontransformed epithelial and carcinoma cells. RSK is sufficient to induce certain motile responses. Expression profiling analysis revealed that a primary role of RSK is to induce transcription of a potent promotile/invasive gene program by FRA1-dependent and -independent mechanisms. The program enables RSK to coordinately modulate the extracellular environment, the intracellular motility apparatus, and receptors mediating communication between these compartments to stimulate motility and invasion. These findings uncover a mechanism whereby the RAS-ERK pathway controls epithelial cell motility by identifying RSK as a key effector, from which emanate multiple highly coordinate transcription-dependent mechanisms for stimulation of motility and invasive properties.

Indexed as

Cell MovementCell TransdifferentiationAnimalsCarcinomaCell LineCell Transformation, NeoplasticDogsEpithelial CellsExtracellular Signal-Regulated MAP KinasesFos-Related Antigen 1Gene Expression ProfilingGene Expression Regulation, NeoplasticGenotypeHumansMesodermNeoplasm InvasivenessExtracellular Signal-Regulated MAP KinasesFos-Related Antigen 1Proto-Oncogene Proteins c-fosras Proteinsribosomal protein S6 kinase, 90kDa, polypeptide 3Ribosomal Protein S6 Kinases, 90-kDaRPS6KA1 protein, human

Identifiers

PMID19716794
PMCPMC3784321
OpenAlexW2160219683

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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.