ArticleMolecular cancer research : MCR2009
BAX/BAK-independent mitoptosis during cell death induced by proteasome inhibition?
Article in Molecular cancer research : MCR, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 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
11 citing papers in PubMed, 32 citations in OpenAlex.
- Tipping the balance of cell death: alternative splicing as a source of MCL-1S in cancer.Cell death & disease · 2024Review
- Roles of Bak and Sirt3 in Paraquat-Induced Cochlear Hair Cell Damage.Neurotoxicity research · 2021Article
- Discovery of Small Molecule Bak Activator for Lung Cancer Therapy.Theranostics · 2021Article
- Molecular analysis of Culex quinquefasciatus larvae responses to Lysinibacillus sphaericus Bin toxin.PloS one · 2017Article
- Prima-1 induces apoptosis in bladder cancer cell lines by activating p53.Clinics (Sao Paulo, Brazil) · 2013Article
- Shikonin induces immunogenic cell death in tumor cells and enhances dendritic cell-based cancer vaccine.Cancer immunology, immunotherapy : CII · 2012Article
- Impairment of the ubiquitin-proteasome pathway by methyl N-(6-phenylsulfanyl-1H-benzimidazol-2-yl)carbamate leads to a potent cytotoxic effect in tumor cells: a novel antiproliferative agent with a potential therapeutic implication.The Journal of biological chemistry · 2012Article
- Article
- Essential requirement of cytochrome c release for caspase activation by procaspase-activating compound defined by cellular models.Cell death & disease · 2011Article
- Inhibition of protein degradation induces apoptosis through a microtubule-associated protein 1 light chain 3-mediated activation of caspase-8 at intracellular membranes.Molecular and cellular biology · 2011Article
- Cumulus Cells Are Potential Candidates for Cell Therapy.In vivo (Athens, Greece)Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Proteasome inhibitors induce rapid death of cancer cells. We show that in epithelial cancer cells, such death is associated with dramatic and simultaneous up-regulation of several BH3-only proteins, including BIK, BIM, MCL-1S, NOXA, and PUMA, as well as p53. Elevated levels of these proteins seem to be the result of direct inhibition of their proteasomal degradation, induction of transcription, and active translation. Subsequent cell death is independent of BAX, and probably BAK, and proceeds through the intrinsic mitochondrial apoptosis pathway. We identify the cascade of molecular events responsible for cell death induced by a prototypical proteasome inhibitor, MG132, starting with rapid accumulation of BH3-only proteins in the mitochondria, proceeding through mitochondrial membrane permeabilization and subsequent loss of DeltaPsi(m), and leading to irreversible changes of mitochondrial ultrastructure, degradation of mitochondrial network, and detrimental impairment of crucial mitochondrial functions. Our results also establish a rationale for the broader use of proteasome inhibitors to kill apoptosis-resistant tumor cells that lack functional BAX/BAK proteins.
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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.