Evidence map›Paper›PMID 30728292›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

ERK2 regulates epithelial-to-mesenchymal plasticity through DOCK10-dependent Rac1/FoxO1 activation.

Sejeong Shin, Gwen R Buel, Michal J Nagiec, Min-Joon Han, Philippe P Roux, John Blenis, Sang-Oh Yoon

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.

0numbers the graph read from it
0cells of the map it votes in
60citing papers in PubMed
7.2field-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

60 citing papers in PubMed, 96 citations in OpenAlex.

  1. Article
  2. Multi-omic Profiling of Recurrence Risk Across Breast Cancer Subtypes.medRxiv : the preprint server for health sciences · 2026
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  3. bioRxiv : the preprint server for biology · 2025
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  4. BRAF inhibition increases TGFβ2 production and stimulates metastasis in mice with endogenous BRAFProceedings of the National Academy of Sciences of the United States of America · 2025
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  18. Retinoblastoma: present scenario and future challenges.Cell communication and signaling : CCS · 2023
    Review
  19. Article
  20. 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 4 institutions in 2 countries.

Sejeong ShinDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine, Peoria, IL 61605.
Gwen R BuelDepartment of Pharmacology, Weill Cornell Medicine, New York, NY 10021.
Michal J NagiecDepartment of Pharmacology, Weill Cornell Medicine, New York, NY 10021.
Min-Joon HanDepartment of Hematology, St. Jude Children's Research Hospital, Memphis, TN 38105.
Philippe P RouxInstitute for Research in Immunology and Cancer, University of Montreal, Montreal, QC H3C 3J7, Canada.ORCID 0000-0002-5962-0250
John BlenisDepartment of Pharmacology, Weill Cornell Medicine, New York, NY 10021; jblenis@med.cornell.edu syoon1@uic.edu.
Sang-Oh YoonDepartment of Cancer Biology and Pharmacology, University of Illinois College of Medicine, Peoria, IL 61605; jblenis@med.cornell.edu syoon1@uic.edu.
Cornell University · USUniversity of Illinois Urbana-Champaign · USInstitute for Research in Immunology and Cancer · CASt. Jude Children's Research Hospital · US

Funding

SIGNAL TRANSDUCTION TO PP70 S6KR01GM051405 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI BLENIS, JOHN · 1995 to 2023
$14.0M
ONCOGENIC REGULATION OF S6 PROTEIN KINASE &CELL GROWTHR01CA046595 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI JOHN BLENIS · 1988 to 2026
$10.6M
Mitogenic and Oncogenic Regulation of ERK/RSK SignalingR37CA046595 · NCI · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI BLENIS, JOHN · 2003 to 2012
$6.4M
Molecular and biochemical basis of LymphangioleiomyomatosisR01HL121266 · NHLBI · WEILL MEDICAL COLL OF CORNELL UNIV · PI BLENIS, JOHN · 2014 to 2017
$2.0M
Canadian Institutes for Health Research MOP-142374Canadian Institutes for Health Research PJT-152995NCI NIH HHS R01 CA046595NCI NIH HHS R37 CA046595NHLBI NIH HHS R01 HL121266NIGMS NIH HHS R01 GM051405
6 · The paper itself

Abstract

ERK is a key coordinator of the epithelial-to-mesenchymal transition (EMT) in that a variety of EMT-inducing factors activate signaling pathways that converge on ERK to regulate EMT transcription programs. However, the mechanisms by which ERK controls the EMT program are not well understood. Through an analysis of the global changes of gene expression mediated by ERK2, we identified the transcription factor FoxO1 as a potential mediator of ERK2-induced EMT, and thus we investigated the mechanism by which ERK2 regulates FoxO1. Additionally, our analysis revealed that ERK2 induced the expression of Dock10, a Rac1/Cdc42 GEF, during EMT. We demonstrate that the activation of the Rac1/JNK signaling axis downstream of Dock10 leads to an increase in FoxO1 expression and EMT. Taken together, our study uncovers mechanisms by which epithelial cells acquire less proliferative but more migratory mesenchymal properties and reveals potential therapeutic targets for cancers evolving into a metastatic disease state.

Indexed as

Cell Line, TumorEpithelial-Mesenchymal TransitionForkhead Box Protein O1Gene Expression RegulationGuanine Nucleotide Exchange FactorsHumansMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 1rac1 GTP-Binding ProteinTranscriptional ActivationDOCK10 protein, humanForkhead Box Protein O1FOXO1 protein, humanGuanine Nucleotide Exchange FactorsMAPK1 protein, humanMitogen-Activated Protein Kinase 1rac1 GTP-Binding ProteinRAC1 protein, humanDock10EMTepithelial-to-mesenchymal transitionERK2FoxO

Identifiers

PMID30728292
PMCPMC6386703
OpenAlexW2913645827

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.