ArticleMolecular and cellular biology2015
Extracellular signal-regulated kinase signaling regulates the opposing roles of JUN family transcription factors at ETS/AP-1 sites and in cell migration.
Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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Who cites it
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.
- Advances in sequencing and omics studies in prostate cancer: unveiling molecular pathogenesis and clinical applications.Frontiers in oncology · 2024Pooled it
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- Extracellular signalling regulates gastrin transcription through site-specific phosphorylation and nuclear redistribution of Menin.bioRxiv : the preprint server for biology · 2026Article
- JUNB and JUND in Urological Cancers: A Literature Review.Current issues in molecular biology · 2025Review
- The transcription factor BATF pioneers the differentiation program of effector CD8Cell reports · 2025Article
- Transcriptome analysis reveals the mechanism of Rhodiola polysaccharide affecting the proliferation of porcine Leydig cells under hypoxia.BMC veterinary research · 2025Article
- ETS Family Transcription Factors in Gastric Cancer and the Role of ELF3 in the Core Metaplasia Transcription Factor Network.Oncology research · 2025Article
- Article
- Neuroprotective Effects of Licochalcone D in Oxidative-Stress-Induced Primitive Neural Stem Cells from Parkinson's Disease Patient-Derived iPSCs.Biomedicines · 2023Article
- JUND Promotes Tumorigenesis via Specifically Binding on Enhancers of Multiple Oncogenes in Cervical Cancer.OncoTargets and therapy · 2023Article
- The histone variant macroH2A1.1 regulates RNA polymerase II-paused genes within defined chromatin interaction landscapes.Journal of cell science · 2022Article
- JunD, not c-Jun, is the AP-1 transcription factor required for Ras-induced lung cancer.JCI insight · 2021Article
- Ras/ERK and PI3K/AKT signaling differentially regulate oncogenic ERG mediated transcription in prostate cells.PLoS genetics · 2021Article
- Fra-1 regulates its target genes via binding to remote enhancers without exerting major control on chromatin architecture in triple negative breast cancers.Nucleic acids research · 2021Article
- EGF Induces Migration Independent of EMT or Invasion in A549 Lung Adenocarcinoma Cells.Frontiers in cell and developmental biology · 2021Article
- Inhibition of FGF and TGF-β Pathways in hESCs Identify STOX2 as a Novel SMAD2/4 Cofactor.Biology · 2020Article
- Catestatin reverses the hypertrophic effects of norepinephrine in H9c2 cardiac myoblasts by modulating the adrenergic signaling.Molecular and cellular biochemistry · 2020Article
- Essential role of JunD in cell proliferation is mediated via MYC signaling in prostate cancer cells.Cancer letters · 2019Article
- Transregulation of microRNA miR-21 promoter by AP-1 transcription factor in cervical cancer cells.Cancer cell international · 2019Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
JUN transcription factors bind DNA as part of the AP-1 complex, regulate many cellular processes, and play a key role in oncogenesis. The three JUN proteins (c-JUN, JUNB, and JUND) can have both redundant and unique functions depending on the biological phenotype and cell type assayed. Mechanisms that allow this dynamic switching between overlapping and distinct functions are unclear. Here we demonstrate that JUND has a role in prostate cell migration that is the opposite of c-JUN's and JUNB's. RNA sequencing reveals that opposing regulation by c-JUN and JUND defines a subset of AP-1 target genes with cell migration roles. cis-regulatory elements for only this subset of targets were enriched for ETS factor binding, indicating a specificity mechanism. Interestingly, the function of c-JUN and JUND in prostate cell migration switched when we compared cells with an inactive versus an active RAS/extracellular signal-regulated kinase (ERK) signaling pathway. We show that this switch is due to phosphorylation and activation of JUND by ERK. Thus, the ETS/AP-1 sequence defines a unique gene expression program regulated by the relative levels of JUN proteins and RAS/ERK signaling. This work provides a rationale for how transcription factors can have distinct roles depending on the signaling status and the biological function in question.
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