ArticleFrontiers in oncology2018
Hypoxia-Inducible Factor-1α Activity as a Switch for Glioblastoma Responsiveness to Temozolomide.
Article in Frontiers in oncology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.
- Glioblastoma multiforme (GBM): An overview of current therapies and mechanisms of resistance.Pharmacological research · 2021Pooled it
- Expanding Microgel Parameters to Model the Tumor Microenvironment and Examine Temozolomide Resistance in Glioblastoma.bioRxiv : the preprint server for biology · 2026Article
- Diphenyl Diselenide and Temozolomide: Downregulation of Inflammatory, Redox, and Tumor-Associated Pathways in Glioblastoma.Biological trace element research · 2026Article
- Review
- Therapeutic Potential of Tetrandrine Compared to Temozolomide in Treating Glioblastoma Multiforme Under Normoxic and Hypoxic Conditions.International journal of molecular sciences · 2026Article
- miRNA675-5p inhibitor's dual role as novel therapeutic alternative or sensitizing treatment in resistant glioma models.Molecular therapy. Nucleic acids · 2026Article
- Glioblastoma Stem Cells and Tumour Microenvironment: Interactions Across Hypoxia, Vasculature and Immune Modulation.International journal of molecular sciences · 2026Review
- Targeting leucine-rich repeat kinase 2 overcomes resistance to oncolytic herpes simplex virus-based therapies in glioblastoma.Nature communications · 2026Article
- Histone demethylase KDM4C confers temozolomide resistance to glioblastoma cells by epigenetically regulating E2F6.Archives of pharmacal research · 2025Article
- Virtual Clinical Trial Reveals Significant Clinical Potential of Targeting Tumor-Associated Macrophages and Microglia to Treat Glioblastoma.CPT: pharmacometrics & systems pharmacology · 2025Article
- It's all downstream from here: RTK/Raf/MEK/ERK pathway resistance mechanisms in glioblastoma.Journal of neuro-oncology · 2025Review
- Article
- Understanding Neovascularization in Glioblastoma: Insights from the Current Literature.International journal of molecular sciences · 2025Review
- The Complexity of Malignant Glioma Treatment.Cancers · 2025Review
- From hormonal immunomodulation to glioblastoma therapy: the emerging role of Ouabain.Frontiers in immunology · 2025Review
- Research progress of drug resistance mechanism of temozolomide in the treatment of glioblastoma.Heliyon · 2024Review
- Multi-scale signaling and tumor evolution in high-grade gliomas.Cancer cell · 2024Article
- Tetralol derivative NNC-55-0396 targets hypoxic cells in the glioblastoma microenvironment: an organ-on-chip approach.Cell death & disease · 2024Article
- The role of chaperone-mediated autophagy in drug resistance.Genetics and molecular biology · 2024Article
- Borneol promotes autophagic degradation of HIF-1α and enhances chemotherapy sensitivity in malignant glioma.PeerJ · 2024Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
rationaleThe activity of the transcription factor, hypoxia-inducible factor (HIF)-1α, is a common driver of a number of the pathways involved in the aggressiveness of glioblastomas (GBMs), and it has been suggested that the reduction in this activity observed, soon after the administration of temozolomide (TMZ), can be a biomarker of an early response in GBM models. As HIF-1α is a tightly regulated protein, studying the processes involved in its downregulation could shed new light on the mechanisms underlying GBM sensitivity or resistance to TMZ.
methodsThe effect of HIF-1α silencing on cell responsiveness to TMZ was assessed in four genetically different human GBM cell lines by evaluating cell viability and apoptosis-related gene balance. LAMP-2A silencing was used to evaluate the contribution of chaperone-mediated autophagy (CMA) to the modulation of HIF-1α activity in TMZ-sensitive and TMZ-resistant cells.
resultsThe results showed that HIF-1α but not HIF-2α activity is associated with GBM responsiveness to TMZ: its downregulation improves the response of TMZ-resistant cells, while blocking CMA-mediated HIF-1α degradation induces resistance to TMZ in TMZ-sensitive cells. These findings are in line with the modulation of crucial apoptosis-related genes.
conclusionOur results demonstrate the central role played by HIF-1α activity in determining the sensitivity or resistance of GBMs to TMZ, and we suggest that CMA is the cellular mechanism responsible for modulating this activity after TMZ treatment.
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