ArticleThe EMBO journal2015
JNK-dependent gene regulatory circuitry governs mesenchymal fate.
Article in The EMBO journal, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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.
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.
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Who cites it
31 citing papers in PubMed, 41 citations in OpenAlex.
- Polydopamine-Coated Surfaces Promote Adhesion, Migration, Proliferation, Chemoresistance, Stemness, and Epithelial-Mesenchymal Transition of Human Prostate Cancer Cell Lines In Vitro via Integrin αInternational journal of molecular sciences · 2026Article
- diaPASEF-Powered Chemoproteomics Enables Deep Kinome Interaction Profiling.Journal of proteome research · 2025Article
- The kinase ERK plays a conserved dominant role in the heterogeneity of epithelial-mesenchymal transition in pancreatic cancer cells.Science signaling · 2025Article
- Oxidized Low-Density Lipoprotein as a Potential Target for Enhancing Immune Checkpoint Inhibitor Therapy in Microsatellite-Stable Colorectal Cancer.Antioxidants (Basel, Switzerland) · 2025Review
- Exploring the Causes of Intervertebral Disc Annulus Fibrosus Impairment.Cellular and molecular bioengineering · 2025Review
- Phosphorylation by JNK switches BRD4 functions.Molecular cell · 2024Article
- GDNF-induced phosphorylation of MUC21 promotes pancreatic cancer perineural invasion and metastasis by activating RAC2 GTPase.Oncogene · 2024Article
- Detecting and dissecting signaling crosstalk via the multilayer network integration of signaling and regulatory interactions.Nucleic acids research · 2024Article
- Plasticity in cell migration modes across development, physiology, and disease.Frontiers in cell and developmental biology · 2024Review
- MAPKs in the early steps of senescence implemEMTation.Frontiers in cell and developmental biology · 2023Article
- A complex epigenome-splicing crosstalk governs epithelial-to-mesenchymal transition in metastasis and brain development.Nature cell biology · 2022Article
- Histone deacetylase 3 promotes alveolar epithelial-mesenchymal transition and fibroblast migration under hypoxic conditions.Experimental & molecular medicine · 2022Article
- Alantolactone exhibits antiproliferative and apoptosis-promoting properties in colon cancer model via activation of the MAPK-JNK/c-Jun signaling pathway.Molecular and cellular biochemistry · 2021Article
- Mnt Represses Epithelial Identity To Promote Epithelial-to-Mesenchymal Transition.Molecular and cellular biology · 2021Article
- Overexpression of DTL enhances cell motility and promotes tumor metastasis in cervical adenocarcinoma by inducing RAC1-JNK-FOXO1 axis.Cell death & disease · 2021Article
- E6-mediated activation of JNK drives EGFR signalling to promote proliferation and viral oncoprotein expression in cervical cancer.Cell death and differentiation · 2021Article
- Article
- C-Jun N-terminal kinase (JNK) pathway activation is essential for dental papilla cells polarization.PloS one · 2021Article
- PMEPA1 facilitates non-small cell lung cancer progression via activating the JNK signaling pathway.Cancer biomarkers : section A of Disease markers · 2021Article
- Unresolved Complexity in the Gene Regulatory Network Underlying EMT.Frontiers in oncology · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The epithelial to mesenchymal transition (EMT) is a biological process in which cells lose cell-cell contacts and become motile. EMT is used during development, for example, in triggering neural crest migration, and in cancer metastasis. Despite progress, the dynamics of JNK signaling, its role in genomewide transcriptional reprogramming, and involved downstream effectors during EMT remain largely unknown. Here, we show that JNK is not required for initiation, but progression of phenotypic changes associated with EMT. Such dependency resulted from JNK-driven transcriptional reprogramming of critical EMT genes and involved changes in their chromatin state. Furthermore, we identified eight novel JNK-induced transcription factors that were required for proper EMT. Three of these factors were also highly expressed in invasive cancer cells where they function in gene regulation to maintain mesenchymal identity. These factors were also induced during neuronal development and function in neuronal migration in vivo. These comprehensive findings uncovered a kinetically distinct role for the JNK pathway in defining the transcriptome that underlies mesenchymal identity and revealed novel transcription factors that mediate these responses during development and disease.
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Registered trials
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.