ArticleOncogene2002
Elevated JNK activation contributes to the pathogenesis of human brain tumors.
Article in Oncogene, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 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.
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Who cites it
48 citing papers in PubMed, 106 citations in OpenAlex.
- Natural Compounds Targeting Oncogenic Signaling Networks in Glioblastoma: Molecular Mechanisms, Translational Advances, and Clinical Perspectives.Brain and behavior · 2026Review
- c-Jun N-Terminal Kinase (JNK) Inhibitor IQ-1S as a Suppressor of Tumor Spheroid Growth.Molecules (Basel, Switzerland) · 2025Article
- Comparison of Niosomal formulation of citrus limon peel extracts and doxorubicin effects on MCF-7 and MDA-MB-231 human breast cancer cells.Scientific reports · 2025Article
- Regulation of Blood-Brain Barrier Permeability via JNK Signaling Pathway: Mechanisms and Potential Therapeutic Strategies for Ischemic Stroke, Alzheimer's Disease and Brain Tumors.Molecules (Basel, Switzerland) · 2025Review
- Regulatory mechanism for the human glioblastoma cell-specific expression of the human GD1c/GT1a/GQ1b synthase (hST8Sia V) gene.Glycoconjugate journal · 2023Article
- Review
- Tumor Drug Concentration and Phosphoproteomic Profiles After Two Weeks of Treatment With Sunitinib in Patients with Newly Diagnosed Glioblastoma.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Expression analysis of progesterone‑regulated miRNAs in cells derived from human glioblastoma.Molecular medicine reports · 2021Article
- JNK signaling as a target for anticancer therapy.Pharmacological reports : PR · 2021Review
- c-Jun NH2-terminal kinase suppression significantly inhibits the growth of transplanted breast tumors in mice.The Journal of international medical research · 2020Article
- TLR-4/Wnt modulation as new therapeutic strategy in the treatment of glioblastomas.Oncotarget · 2018Article
- RUNX1 Regulates Migration, Invasion, and Angiogenesis via p38 MAPK Pathway in Human Glioblastoma.Cellular and molecular neurobiology · 2017Article
- Adhesion- and stress-related adaptation of glioma radiochemoresistance is circumvented by β1 integrin/JNK co-targeting.Oncotarget · 2017Article
- Phosphorylation of Glutathione S-Transferase P1 (GSTP1) by Epidermal Growth Factor Receptor (EGFR) Promotes Formation of the GSTP1-c-Jun N-terminal kinase (JNK) Complex and Suppresses JNK Downstream Signaling and Apoptosis in Brain Tumor Cells.The Journal of biological chemistry · 2015Article
- Ligand-Independent EGFR Signaling.Cancer research · 2015Review
- p75 neurotrophin receptor cleavage by α- and γ-secretases is required for neurotrophin-mediated proliferation of brain tumor-initiating cells.The Journal of biological chemistry · 2014Article
- Regulation of protein translation and c-Jun expression by prostate tumor overexpressed 1.Oncogene · 2014Article
- The structural pathway of interleukin 1 (IL-1) initiated signaling reveals mechanisms of oncogenic mutations and SNPs in inflammation and cancer.PLoS computational biology · 2014Article
- JNK signalling in cancer: in need of new, smarter therapeutic targets.British journal of pharmacology · 2014Review
- JNK Signaling in the Control of the Tumor-Initiating Capacity Associated with Cancer Stem Cells.Genes & cancer · 2013Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ERK pathway is typically associated with activation of the EGF receptor and has been shown to play a major role in promoting several tumor phenotypes. An analogous signaling module, the JNK pathway, has not been shown to be consistently activated by the EGF receptor but is instead more uniformly stimulated by cellular stresses and cytokines. The function of the JNK pathway in primary tumors is unclear as it has been implicated in both promoting apoptosis and cell growth in vitro, which may be a reflection of the cell lines chosen. Primary human brain tumors frequently show overexpression of the EGF receptor. To clarify the role of JNK in tumorigenesis, we have investigated the role of JNK in a large panel of primary human brain tumors and tumor derived cell lines. Here we present evidence that JNK has a major role in promoting tumorigenesis both in vivo and in vitro. Western blot analysis demonstrated that 86% (18 of 21) of primary brain tumors showed evidence of JNK activation but only 38% (8 of 21) showed evidence of ERK activation. Kinase assays revealed that 77% of brain tumor cell lines activated JNK in response to EGF (7 of 13) or had high levels of basal activity (3 of 13), whereas none of six normal cell lines analysed, including astrocytes, had these properties. Of several growth factors examined, EGF produced the highest level of JNK induction in tumor cell lines and the duration of activation was greater than that seen for ERK. Expression of a dominant-negative (dn) form of JNK potently inhibited EGF mediated anchorage independent growth and protection from cell death in two glial tumor cell lines. These findings demonstrate that enhanced JNK activation is frequently found in primary brain tumors and that this activation contributes to phenotypes related to transformation.
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What Socratic holds
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 Socratic graph.