ArticleThe Biochemical journal2012
Thioredoxin reductase 1 deficiency enhances selenite toxicity in cancer cells via a thioredoxin-independent mechanism.
Article in The Biochemical journal, 2012. 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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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Genetic Variations Associated with Anti-Tuberculosis Drug-Induced Liver Injury.Current pharmacology reports · 2018Article
- Glutathione peroxidase 4 overexpression inhibits ROS-induced cell death in diffuse large B-cell lymphoma.Laboratory investigation; a journal of technical methods and pathology · 2018Article
- ROS-modulated therapeutic approaches in cancer treatment.Journal of cancer research and clinical oncology · 2017Review
- TXNRD1 Is an Unfavorable Prognostic Factor for Patients with Hepatocellular Carcinoma.BioMed research international · 2017Article
- Multidrug Resistance-associated Protein-1 (MRP-1)-dependent Glutathione Disulfide (GSSG) Efflux as a Critical Survival Factor for Oxidant-enriched Tumorigenic Endothelial Cells.The Journal of biological chemistry · 2016Article
- EF24 induces ROS-mediated apoptosis via targeting thioredoxin reductase 1 in gastric cancer cells.Oncotarget · 2016Article
- Differential acute effects of selenomethionine and sodium selenite on the severity of colitis.Nutrients · 2015Article
- Selenium and selenocysteine: roles in cancer, health, and development.Trends in biochemical sciences · 2014Review
- Regulation of HIF-1α activity by overexpression of thioredoxin is independent of thioredoxin reductase status.Molecules and cells · 2013Article
- Abrogated thioredoxin system causes increased sensitivity to TNF-α-induced apoptosis via enrichment of p-ERK 1/2 in the nucleus.PloS one · 2013Article
- Deletion of thioredoxin reductase and effects of selenite and selenate toxicity in Caenorhabditis elegans.PloS one · 2013Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Selenium is an essential trace element in mammals, but is toxic at high levels. It is best known for its cancer prevention activity, but cancer cells are more sensitive to selenite toxicity than normal cells. Since selenite treatment leads to oxidative stress, and the Trx (thioredoxin) system is a major antioxidative system, we examined the interplay between TR1 (Trx reductase 1) and Trx1 deficiencies and selenite toxicity in DT cells, a malignant mouse cell line, and the corresponding parental NIH 3T3 cells. TR1-deficient cells were far more sensitive to selenite toxicity than Trx1-deficient or control cells. In contrast, this effect was not seen in cells treated with hydrogen peroxide, suggesting that the increased sensitivity of TR1 deficiency to selenite was not due to oxidative stress caused by this compound. Further analyses revealed that only TR1-deficient cells manifested strongly enhanced production and secretion of glutathione, which was associated with increased sensitivity of the cells to selenite. The results suggest a new role for TR1 in cancer that is independent of Trx reduction and compensated for by the glutathione system. The results also suggest that the enhanced selenite toxicity of cancer cells and simultaneous inhibition of TR1 can provide a new avenue for cancer therapy.
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