ArticleStem cell research2014
uPAR and cathepsin B-mediated compartmentalization of JNK regulates the migration of glioma-initiating cells.
Article in Stem cell research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- MAP3K1: A Multifunctional Kinase at the Crossroads of Cancer Progression and Tumor Suppression.Cells · 2026Review
- Arrestin-3 sca-olds multiple MAP3Ks driving stress-induced JNK3 activation and cell death.bioRxiv : the preprint server for biology · 2026Article
- Review
- Vincristine exerts antiglioma effects by inhibiting the PI3K/AKT signaling pathway: A mechanistic study based on network pharmacology, bioinformatics analysis, and experimental validation.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Network pharmacology-based strategy to investigate the effect and mechanism of α-solanine against glioma.BMC complementary medicine and therapies · 2023Article
- Neuronal Death Caused by HMGB1-Evoked via Inflammasomes from Thrombin-Activated Microglia Cells.International journal of molecular sciences · 2023Article
- The role of lysosomal peptidases in glioma immune escape: underlying mechanisms and therapeutic strategies.Frontiers in immunology · 2023Review
- Lysosomal peptidases-intriguing roles in cancer progression and neurodegeneration.FEBS open bio · 2022Review
- Proteases Regulate Cancer Stem Cell Properties and Remodel Their Microenvironment.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2021Review
- Role of lysosomes in physiological activities, diseases, and therapy.Journal of hematology & oncology · 2021Review
- Investigating Glioblastoma Response to Hypoxia.Biomedicines · 2020Article
- Morphological and Molecular Changes in Juvenile Normal Human Fibroblasts Exposed to Simulated Microgravity.Scientific reports · 2019Article
- Identification of Key Pathways and Genes in the Orai2 Mediated Classical and Mesenchymal Subtype of Glioblastoma by Bioinformatic Analyses.Disease markers · 2019Article
- Localization patterns of cathepsins K and X and their predictive value in glioblastoma.Radiology and oncology · 2018Article
- Over-expression of cathepsin B in hepatocellular carcinomas predicts poor prognosis of HCC patients.Molecular cancer · 2016Article
- Cathepsin B Expression and the Correlation with Clinical Aspects of Oral Squamous Cell Carcinoma.PloS one · 2016Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
In the present study, we investigated the effect of simultaneous downregulation of uPAR and cathepsin B (pUC), alone or in combination with radiation, on JNK-MAPK signaling pathway in regulating the migration of non-GICs (glioma-initiating cells) and GICs. The increase in the expression of p-JNK with pUC treatment was mostly localized to nucleus whereas increase in the expression of p-JNK with radiation and overexpression of uPAR and cathepsin B was confined to cytoplasm of the cells. Depletion of cytosolic p-JNK with pUC treatment inhibited migration by downregulating the expression of the adapter proteins of the focal adhesion complex. We also observed that knockdown of uPAR and cathepsin B regulated the Ras-Pak-1 pathway to induce the translocation of p-JNK from cytosol to nucleus. In control cells, Pak-1 served as a functional inhibitor for MEKK-1, which inhibits the complex formation of MEKK-1 and p-JNK and thus inhibits the translocation of this complex into nucleus. Hence, we conclude that glioma cells utilize the availability of cytosolic p-JNK in driving the cells towards migration. Finally, treating the cells with pUC alone or in combination with radiation induced the translocation of the MEKK-1-p-JNK complex from cytosol to nucleus, thereby inhibiting the migration of glioma cells.
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