ArticleCell death & disease2013
BNIP3 acts as transcriptional repressor of death receptor-5 expression and prevents TRAIL-induced cell death in gliomas.
Article in Cell death & disease, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- Molecular regulation of mitophagy signaling in tumor microenvironment and its targeting for cancer therapy.Cytokine & growth factor reviews · 2025Review
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Molecular signatures in prion disease: altered death receptor pathways in a mouse model.Journal of translational medicine · 2024Article
- BNIP3 as a new tool to promote healthy brain aging.Aging cell · 2024Review
- Prognostic signature based on mitochondria quality control proteins for the prediction of lung adenocarcinoma patients survival.Cell death discovery · 2023Article
- Multifaceted roles of mitochondria in wound healing and chronic wound pathogenesis.Frontiers in cell and developmental biology · 2023Review
- Autophagy inhibition by TSSC4 (tumor suppressing subtransferable candidate 4) contributes to sustainable cancer cell growth.Autophagy · 2022Article
- The Role of Micro RNAs in Regulating PI3K/AKT Signaling Pathways in Glioblastoma.Iranian journal of pathology · 2022Review
- Article
- Investigating Glioblastoma Response to Hypoxia.Biomedicines · 2020Article
- Bnip3 regulates airway smooth muscle cell focal adhesion and proliferation.American journal of physiology. Lung cellular and molecular physiology · 2019Article
- Autophagic and Apoptotic Pathways as Targets for Chemotherapy in Glioblastoma.International journal of molecular sciences · 2018Review
- MicroRNA-145 induces apoptosis of glioma cells by targeting BNIP3 and Notch signaling.Oncotarget · 2017Article
- Intracellular localization of DR5 and related regulatory pathways as a mechanism of resistance to TRAIL in cancer.Cellular and molecular life sciences : CMLS · 2017Review
- Repurposing L-Menthol for Systems Medicine and Cancer Therapeutics? L-Menthol Induces Apoptosis through Caspase 10 and by Suppressing HSP90.Omics : a journal of integrative biology · 2016Article
- Dual Agonist Surrobody Simultaneously Activates Death Receptors DR4 and DR5 to Induce Cancer Cell Death.Molecular cancer therapeutics · 2016Article
- Inhibition of Notch1 signaling overcomes resistance to the death ligand Trail by specificity protein 1-dependent upregulation of death receptor 5.Cell death & disease · 2015Article
- TAp73 transcriptionally represses BNIP3 expression.Cell cycle (Georgetown, Tex.) · 2015Article
- Bnip3 Binds and Activates p300: Possible Role in Cardiac Transcription and Myocyte Morphology.PloS one · 2015Article
- Phosphorylation of the BNIP3 C-Terminus Inhibits Mitochondrial Damage and Cell Death without Blocking Autophagy.PloS one · 2015Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glioblastoma multiforme (GBM) is the most common and malignant brain tumor, and current treatment modalities such as surgical resection, adjuvant radiotherapy and temozolomide (TMZ) chemotherapy are ineffective. Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a novel cancer therapeutic agent for GBM because of its capability of inducing apoptosis in glioma cells. Unfortunately, the majority of glioma cells are resistant to TRAIL-induced apoptosis. The Bcl-2 nineteen kilodalton interacting protein (BNIP3) is a pro-cell death BH3-only member of the Bcl-2 family that is one of the highest expressed genes in hypoxic regions of GBM tumors. We previously found that BNIP3 is localized to the nucleus in GBM tumors and suppresses cell death in glioma cells. Herein, we have discovered when BNIP3 nuclear expression is knockdown in glioma cell lines and in normal mouse astrocytes, TRAIL and its death receptor, death receptor-5 (DR5) expression is increased. In addition, when nuclear BNIP3 expression is increased, the amount of TRAIL-induced apoptosis is reduced. Using a streptavidin pull-down assay, we found that BNIP3 binds to the DR5 promoter and nuclear BNIP3 binds to the DR5 promoter. Furthermore, nuclear BNIP3 expression in GBM tumors correlates with decreased DR5 expression. Taken together, we have discovered a novel transcriptional repression function for BNIP3 conferring a TRAIL resistance in glioma cells.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.