ArticleCancer medicine2021
DYRK1A activates NFATC1 to increase glioblastoma migration.
Article in Cancer medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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The trial behind it
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Transcranial direct current stimulation enhances cognitive performance and modulates QEEG beta- and theta-band power in patients undergoing whole-brain radiotherapy.IBRO neuroscience reports · 2026Article
- Integrative Insights Into DYRK1A From Molecular Function to Therapeutic Advancement.Chemical biology & drug design · 2026Review
- Small-molecule inhibitors of the protein kinase DYRK as potential therapeutic candidates in cancer.Cell chemical biology · 2026Article
- Nuclear Factor of Activated T Cells (NFAT) Proteins as Targeted Molecules in Diseases: A Narrative Review.Cureus · 2024Review
- DYRK1A-mediated PLK2 phosphorylation regulates the proliferation and invasion of glioblastoma cells.International journal of oncology · 2023Article
- New insights into the roles for DYRK family in mammalian development and congenital diseases.Genes & diseases · 2023Review
- Systematic analysis identifies REST as an oncogenic and immunological biomarker in glioma.Scientific reports · 2023Article
- DYRK1A reinforces epithelial-mesenchymal transition and metastasis of hepatocellular carcinoma via cooperatively activating STAT3 and SMAD.Journal of biomedical science · 2022Article
- A Bioinformatics Evaluation of the Role of Dual-Specificity Tyrosine-Regulated Kinases in Colorectal Cancer.Cancers · 2022Article
- DYRK1A activates NFATC1 to increase glioblastoma migration.Cancer medicine · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Glioblastoma (GBM) is the most aggressive glioma, and is prone to develop resistance to chemotherapy and radiotherapy; hence, patients with glioblastoma have a high recurrence rate and a low 1-year survival rate. In addition, the pathogenesis of glioblastoma is complex and largely unknown, and the available treatments are limited. Here, we uncovered a fundamental role of DYRK1A in regulating NFATC1 in GBMs. We found that DYRK1A was highly expressed in glioma and glioblastoma cells, and its expression was positively correlated with that of NFATC1. Moreover, inhibition of DYRK1A promoted NFATC1 degradation in GBM cells and sharply reduced the transactivation of NFATC1, not only by decreasing the expression of NFATC1-targeted genes, but also by reducing the luciferase activity, and vice versa. However, DYRK1A had the opposite effect on NFATC2. Most importantly, our data suggest that DYRK1A inhibition reduces glioblastoma migration. Polypeptides derived from the DYRK1A-targeted motif of NFATC1, by competitively blocking DYRK1A kinase activity on NFATC1, clearly destabilized NFATC1 protein and impaired glioblastoma migration. We propose that the recovery of NFATC1 stability is a key oncogenic event in a large proportion of gliomas, and pharmacological inhibition of DYRK1A by polypeptides could represent a promising therapeutic intervention for GBM.
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Registered trials
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