ArticleOncology research2023
Mechanism of NURP1 in temozolomide resistance in hypoxia-treated glioma cells via the KDM3A/TFEB axis.
Article in Oncology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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Who cites it
6 citing papers in PubMed, 12 citations in OpenAlex.
- MGMT, NUPR1, NDRG2, and GLI1 Gene Promoter Methylation in Glioblastoma Tissues and Association with Clinical Characteristics and Therapeutic Outcomes.International journal of molecular sciences · 2026Article
- Targeting intrinsically disordered nuclear protein 1 (NUPR1) with single-domain antibodies alleviates triple-negative breast cancer (TNBC) progression in vivo.Cell death & disease · 2025Article
- Licochalcone A inhibits glioma migration, invasion, and growth by triggering mitochondrial dysfunction and ROS-mediated oxidative damage.Molecular and cellular biochemistry · 2025Article
- Proteomic Analysis Uncovers Enhanced Inflammatory Phenotype and Distinct Metabolic Changes in IDH1 Mutant Glioma Cells.International journal of molecular sciences · 2025Article
- Hypoxia-Inducible Factor-Dependent and Independent Mechanisms Underlying Chemoresistance of Hypoxic Cancer Cells.Cancers · 2024Review
- Developing risk models and subtypes of autophagy-associated LncRNAs for enhanced prognostic prediction and precision in therapeutic approaches for liver cancer patients.Oncology research · 2024Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Temozolomide (TMZ) resistance is a major obstacle in glioma treatment. Nuclear protein-1 (NUPR1) is a regulator of glioma progression. This study investigated the mechanism of NUPR1 in TMZ resistance in hypoxia-treated glioma cells and its mechanism in modulating autophagy. We treated TMZ-resistant cells U251-TMZ and T98G-TMZ to normoxia or hypoxia and silenced NUPR1 in hypoxia-treated U251-TMZ and T98G-TMZ cells to assess cell viability, proliferation, apoptosis, LC3-II/LC3-I and p62 expressions, and autophagic flux under different concentrations of TMZ. We found that hypoxia upregulated NUPR1 expression and autophagy while NUPR1 silencing suppressed hypoxia-induced TMZ resistance and autophagy in glioma cells. We also investigated the interaction between NUPR1 and lysine demethylase 3A (KDM3A), as well as the enrichments of KDM3A and H3 lysine 9 dimethylation (H3K9me2) in the transcription factor EB (TFEB) promoter region. Our results suggest that hypoxia-induced NUPR1 promotes TFEB transcription by binding to KDM3A and reducing H3K9me2 levels, thereby augmenting glioma cell autophagy and TMZ resistance. Moreover, the overexpression of KDM3A or TFEB promoted glioma cell autophagy. In a xenograft tumor model, silencing NUPR1 suppressed TMZ resistance in glioma cells
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