Mitochondrial thioredoxin reductase regulates major cytotoxicity pathways of proteasome inhibitors in multiple myeloma cells
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Summary
A mechanism underlying the ability of proteasome inhibitors bortezomib and carfilzomib to directly induce oxidative and ER stresses in multiple myeloma cells via transcriptional repression of a gene encoding mitochondrial thioredoxin reductase (TXNRD2) is reported.
- Type
- article
- Published
- 2015-07-24
- Cited by
- 56
- References
- 46
- Access
- Open access
- OpenAlex
- https://openalex.org/W1920908631
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:21240675
Keywords
Carfilzomib, Bortezomib, Proteasome, Oxidative stress, Thioredoxin reductase
References
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- Targeting the insulin-like growth factor-1 receptor to overcome bortezomib resistance in preclinical models of multiple myeloma.
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- Proteasome inhibitors induce a terminal unfolded protein response in multiple myeloma cells.
- Persistent oxidative stress in cancer
- Gene expression analysis of B‐lymphoma cells resistant and sensitive to bortezomib *
- Nrf2 amplifies oxidative stress via induction of Klf9
- Role of oxidative stress and intracellular glutathione in the sensitivity to apoptosis induced by proteasome inhibitor in thyroid cancer cells
Cited by
- Oxidative Stress and Proteasome Inhibitors in Multiple Myeloma
- Mitochondrial Redox Signaling and Tumor Progression
- Carfilzomib triggers cell death in chronic lymphocytic leukemia by inducing proapoptotic and endoplasmic reticulum stress responses
- EM23, A Natural Sesquiterpene Lactone from Elephantopus mollis, Induces Apoptosis in Human Myeloid Leukemia Cells through Thioredoxin- and Reactive Oxygen Species-Mediated Signaling Pathways
- Endoplasmic-reticulum stress pathway-associated mechanisms of action of proteasome inhibitors in multiple myeloma
- Microphthalmia-Associated Transcription Factor Suppresses Invasion by Reducing Intracellular GTP Pools
- Cyclin D1 unbalances the redox status controlling cell adhesion, migration, and drug resistance in myeloma cells
- Human MutT homologue 1 mRNA overexpression correlates to poor response of multiple myeloma
- Multiple myeloma cells' capacity to decompose H2O2 determines lenalidomide sensitivity.
- Mitochondrial ROS Control of Cancer
- The Role of NOX4 and TRX2 in Angiogenesis and Their Potential Cross-Talk
- Altered expression of mitochondrial antioxidants in oral squamous cell carcinoma.
- High NRF2 expression controls endoplasmic reticulum stress induced apoptosis in multiple myeloma.
- Mitochondrial targeted curcumin exhibits anticancer effects through disruption of mitochondrial redox and modulation of TrxR2 activity
- Selenoproteins in colon cancer
- Resveratrol Sensitizes Carfilzomib-Induced Apoptosis via Promoting Oxidative Stress in Multiple Myeloma Cells
- Generation and characterisation of human embryonic stem cells deficient in ZDHHC8, a gene deleted in 22q11.2 deletion syndrome
- Inhibition of the aryl hydrocarbon receptor/polyamine biosynthesis axis suppresses multiple myeloma
- The Association of Neuronal Stress with Activating Transcription Factor 3 in Dorsal Root Ganglion of in vivo and in vitro Models of Bortezomib- Induced Neuropathy.
- Scutellarein selectively targets multiple myeloma cells by increasing mitochondrial superoxide production and activating intrinsic apoptosis pathway.
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- Perturbation of redox balance after thioredoxin reductase deficiency interrupts autophagy-lysosomal degradation pathway and enhances cell death in nutritionally stressed SH-SY5Y cells.