ArticleProceedings of the National Academy of Sciences of the United States of America2008
Bcl2L12-mediated inhibition of effector caspase-3 and caspase-7 via distinct mechanisms in glioblastoma.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 82 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
82 citing papers in PubMed, 145 citations in OpenAlex.
- A first-in-human phase 0 clinical study of RNA interference-based spherical nucleic acids in patients with recurrent glioblastoma.Science translational medicine · 2021Trial
- Caspases as master regulators of programmed cell death: apoptosis, pyroptosis and beyond.Experimental & molecular medicine · 2025Review
- Protein phosphatase EYA1 regulates the dephosphorylation and turnover of BCL2L12 to promote glioma development.International journal of biological sciences · 2025Article
- Citronellol Induces Apoptosis via Differential Regulation of Caspase-3, NF-κB, and JAK2 Signaling Pathways in Glioblastoma Cell Line.Food science & nutrition · 2025Article
- Splicing factor SRSF1 attenuates cardiomyocytes apoptosis via regulating alternative splicing of Bcl2L12.Cell & bioscience · 2024Article
- Plasma alpha B crystallin as potential biomarker for predicting pre-operative seizures in glioma.BMC neurology · 2024Article
- Differential Proteome Profiling Analysis under Pesticide Stress by the Use of a Nano-UHPLC-MS/MS Untargeted Proteomic-Based Approach on a 3D-Developed Neurospheroid Model: Identification of Protein Interactions, Prognostic Biomarkers, and Potential Therapeutic Targets in Human IDH Mutant High-Grade Gliomas.Journal of proteome research · 2023Article
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- Multi-omics-based analysis of high grade serous ovarian cancer subtypes reveals distinct molecular processes linked to patient prognosis.FEBS open bio · 2023Article
- Nucleic acid drug vectors for diagnosis and treatment of brain diseases.Signal transduction and targeted therapy · 2023Review
- Antineoplastic multi-drug chemotherapy to sensitize tumors triggers multi-drug resistance and inhibits efficiency of maintenance treatment inglioblastoma cells.EXCLI journal · 2023Article
- Splicing factor BUD31 promotes ovarian cancer progression through sustaining the expression of anti-apoptotic BCL2L12.Nature communications · 2022Article
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- Spherical Nucleic Acids as Precision Therapeutics for the Treatment of Cancer-From Bench to Bedside.Cancers · 2022Review
- PEGylation and folic-acid functionalization of cationic lipoplexes-Improved nucleic acid transfer into cancer cells.Frontiers in bioengineering and biotechnology · 2022Article
- Transcriptomics-Based Investigation of Molecular Mechanisms Underlying Apoptosis Induced by ZnO Nanoparticles in Human Diffuse Large B-Cell Lymphoma.International journal of nanomedicine · 2022Article
- Cytotoxicity and changes in gene expression under aluminium potassium sulfate on Spodoptera frugiperda 9 cells.Ecotoxicology (London, England) · 2021Article
- Effect of Structural Changes Induced by Deletion ofInternational journal of molecular sciences · 2021Article
- In vivo Engineering of Chromosome 19 q-arm by Employing the CRISPR/AsCpf1 and ddAsCpf1 Systems in Human Malignant Gliomas (Hypothesis).Journal of molecular neuroscience : MN · 2021Article
22 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
Glioblastoma multiforme (GBM) is a highly aggressive brain cancer that is characterized by the paradoxical features of intense apoptosis resistance yet a marked propensity to undergo necrosis. Bcl2L12 (for Bcl2-Like12) is a nuclear and cytoplasmic oncoprotein that is universally overexpressed in primary GBM and functions to block postmitochondrial apoptosis signaling by neutralizing effector caspase-3 and caspase-7 maturation. This postmitochondrial block in apoptosis engenders the alternate cell fate of cellular necrosis, thus providing a molecular explanation for GBM's classical features. Whereas Bcl2L12-mediated neutralization of caspase-7 maturation involves physical interaction, the mechanism governing Bcl2L12-mediated inhibition of caspase-3 activity is not known. The nuclear localization of Bcl2L12 prompted expression profile studies of primary astrocytes engineered to overexpress Bcl2L12. The Bcl2L12 transcriptome revealed a striking induction of the small heat shock protein alpha-basic-crystallin (alphaB-crystallin/HspB5), a link reinforced by robust alphaB-crystallin expression in Bcl2L12-expressing orthotopic glioma and strong coexpression of alphaB-crystallin and Bcl2L12 proteins in human primary GBMs. On the functional level, enforced alphaB-crystallin or Bcl2L12 expression enhances orthotopic tumor growth. Conversely, RNAi-mediated knockdown of alphaB-crystallin in Bcl2L12-expressing astrocytes and glioma cell lines with high endogenous alphaB-crystallin showed enhanced apoptosis, yet decreased necrotic cell death with associated increased caspase-3 but not caspase-7 activation. Mirroring this specific effect on effector caspase-3 activation, alphaB-crystallin selectively binds pro-caspase-3 and its cleavage intermediates in vitro and in vivo. Thus, alphaB-crystallin is a Bcl2L12-induced oncoprotein that enables Bcl2L12 to block the activation of both effector caspases via distinct mechanisms, thereby contributing to GBM pathogenesis and its hallmark biological properties.
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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.