ArticleNeuro-oncology2020
NFAT2-HDAC1 signaling contributes to the malignant phenotype of glioblastoma.
Article in Neuro-oncology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 44 citations in OpenAlex.
- Nuclear factor of activated T cells as a driver of tumor progression and a target for precision therapy.Animal models and experimental medicine · 2026Review
- Tumor Electric Field Therapy Inhibits TGF-β/C1R Signaling Axis-Driven Epithelial-Mesenchymal Transition in Glioblastoma.CNS neuroscience & therapeutics · 2026Article
- Phenotypic variations in glioma stem cells: regulatory mechanisms and implications for therapeutic strategies.Journal of translational medicine · 2025Review
- Exploring the potential mechanisms of acetyl tributyl citrate exposure on osteoarthritis based on novel network toxicology.Scientific reports · 2025Article
- NFATc1 facilitates hepatocellular carcinoma progression by regulating the senescence-associated secretory phenotype.Scientific reports · 2025Article
- Epigenetic regulation of histone modifications in glioblastoma: recent advances and therapeutic insights.Biomarker research · 2025Review
- The role of SPI1/VSIG4/THBS1 on glioblastoma progression through modulation of the PI3K/AKT pathway.Journal of advanced research · 2025Article
- Emerging roles of CircRNA-miRNA networks in cancer development and therapeutic response.Non-coding RNA research · 2025Review
- CCN1 Promotes Mesenchymal Phenotype Transition Through Activating NF-κB Signaling Pathway Regulated by S100A8 in Glioma Stem Cells.CNS neuroscience & therapeutics · 2024Article
- Neuronal Differentiation of Human Glioma Cells Induced by Parthenolide Under In Vitro Conditions.Biomedicines · 2024Article
- CCL2 mediated IKZF1 expression promotes M2 polarization of glioma-associated macrophages through CD84-SHP2 pathway.Oncogene · 2024Article
- Comprehensive understanding of glioblastoma molecular phenotypes: classification, characteristics, and transition.Cancer biology & medicine · 2024Review
- USP7-mediated JUND suppresses RCAN2 transcription and elevates NFATC1 to enhance stem cell property in colorectal cancer.Cell biology and toxicology · 2023Article
- Transcriptional Profiling of a Patient-Matched Cohort of Glioblastoma (IDH-Wildtype) for Therapeutic Target and Repurposing Drug Identification.Biomedicines · 2023Article
- SPI1-mediated MIR222HG transcription promotes proneural-to-mesenchymal transition of glioma stem cells and immunosuppressive polarization of macrophages.Theranostics · 2023Article
- Circular RNA circPTPRF promotes the progression of GBM via sponging miR-1208 to up-regulate YY1.Cancer cell international · 2022Article
- Loss of deubiquitylase USP2 triggers development of glioblastoma via TGF-β signaling.Oncogene · 2022Article
- The role of protein acetylation in carcinogenesis and targeted drug discovery.Frontiers in endocrinology · 2022Review
- Circular RNA circASPM promotes the progression of glioblastoma by acting as a competing endogenous RNA to regulate miR-130b-3p/E2F1 axis.Journal of Cancer · 2022Article
- TOPK Affects Autophagy of Skin Squamous Cell Carcinoma by Regulating NF-KB Pathway through HDAC1.Disease markers · 2022Article
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7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDeregulation of the nuclear factor of activated T cell (NFAT) pathway has been reported in several human cancers. Particularly, NFAT2 is involved in the malignant transformation of tumor cells and is identified as an oncogene. However, the role of NFAT2 in glioblastoma (GBM) is largely unknown.
methodsThe expression and prognostic value of NFAT2 were examined in the databases of the Repository of Molecular Brain Neoplasia Data and The Cancer Genome Atlas (TCGA) and clinical samples. The functional effects of silencing or overexpression of NFAT2 were evaluated in glioma stem cell (GSC) viability, invasion, and self-renewal in vitro and in tumorigenicity in vivo. The downstream target of NFAT2 was investigated.
resultsHigh NFAT2 expression was significantly associated with mesenchymal (MES) subtype and recurrent GBM and predicted poor survival. NFAT2 silencing inhibited the invasion and clonogenicity of MES GSC-enriched spheres in vitro and in vivo. NFAT2 overexpression promoted tumor growth and MES differentiation of GSCs. A TCGA database search showed that histone deacetylase 1 (HDAC1) expression was significantly correlated with that of NFAT2. NFAT2 regulates the transcriptional activity of HDAC1. Rescue of HDAC1 in NFAT2-knockdown GSCs partially restored tumor growth and MES phenotype. Loss of NFAT2 and HDAC1 expression resulted in hyperacetylation of nuclear factor-kappaB (NF-κB), which inhibits NF-κB-dependent transcriptional activity.
conclusionOur findings suggest that the NFAT2-HDAC1 pathway might play an important role in the maintenance of the malignant phenotype and promote MES transition in GSCs, which provide potential molecular targets for the treatment of GBMs.
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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.