ArticleBiochemical and biophysical research communications2016
Bortezomib sensitizes human glioblastoma cells to induction of apoptosis by type I interferons through NOXA expression and Mcl-1 cleavage.
Article in Biochemical and biophysical research communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- Apolipoprotein D downregulation in OSCC: multi-database validation and clinical significance.BMC medical genomics · 2026Article
- PMAIP1 promotes J subgroup avian leukosis virus replication by regulating mitochondrial function.Poultry science · 2024Article
- Molecular Insights and Prognosis Associated With RBM8A in Glioblastoma.Frontiers in molecular biosciences · 2022Article
- Noxa and Puma genes regulated by hTERT promoter can mitigate growth and induce apoptosis in hepatocellular carcinoma mouse model.Journal of Cancer · 2022Article
- Aspirin Induced Glioma Apoptosis through Noxa Upregulation.International journal of molecular sciences · 2020Article
- [Effect of bortezomib in inducing apoptosis of imatinib-resistant K562 cells and the mechanism].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2017Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
Glioblastomas are highly invasive and aggressive primary brain tumors. Type I interferons have significant, pleiotropic anticancer activity. However, through various pathways many cancers become interferon-resistant, limiting interferon's clinical utility. In this study, we demonstrated that the proteasomal inhibitor bortezomib sensitized human glioblastoma cells to the antiproliferative action of interferons, which involved the induction of caspase-dependent apoptosis but not necroptosis. We found that death ligands such as TRAIL (TNF-related apoptosis-inducing ligand) were not involved in interferon/bortezomib-induced apoptosis, although interferon induced TRAIL expression. However, apoptosis was induced through an intrinsic pathway involving increased NOXA expression and Mcl-1 cleavage. Our findings may provide an important rationale for combining type I interferons with bortezomib for glioblastoma therapy.
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Registered trials
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