ArticleMolecular and cellular biology2006
Nitrosylcobalamin promotes cell death via S nitrosylation of Apo2L/TRAIL receptor DR4.
Article in Molecular and cellular biology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 67 citations in OpenAlex.
- Article
- Article
- CD320 Receptor and Vitamin B12 as Potential Targets for Anti-Cancer Therapy.International journal of molecular sciences · 2025Review
- The evolution of S-nitrosylation detection methodology and the role of protein S-nitrosylation in various cancers.Cancer cell international · 2024Review
- A metabolic perspective on nitric oxide function in melanoma.Biochimica et biophysica acta. Reviews on cancer · 2024Review
- Nitroglycerin: a comprehensive review in cancer therapy.Cell death & disease · 2023Review
- Protein post-translational modifications in the regulation of cancer hallmarks.Cancer gene therapy · 2023Review
- A20 Restricts NOS2 Expression and Intestinal Tumorigenesis in a Mouse Model of Colitis-Associated Cancer.Gastro hep advances · 2023Article
- S-Nitrosylation in Tumor Microenvironment.International journal of molecular sciences · 2021Review
- The human BThe Journal of biological chemistry · 2020Article
- Targeting apoptosis in cancer therapy.Nature reviews. Clinical oncology · 2020Review
- Review
- Oxidants, Antioxidants and Thiol Redox Switches in the Control of Regulated Cell Death Pathways.Antioxidants (Basel, Switzerland) · 2020Review
- Vitamin BBiomolecules · 2020Article
- The dichotomous role of HBiochemical pharmacology · 2018Review
- S-Nitrosylation in TNF superfamily signaling pathway: Implication in cancer.Redox biology · 2015Review
- S-Nitrosoglutathione-mediated STAT3 regulation in efficacy of radiotherapy and cisplatin therapy in head and neck squamous cell carcinoma.Redox biology · 2015Article
- Regulation of cell death receptor S-nitrosylation and apoptotic signaling by Sorafenib in hepatoblastoma cells.Redox biology · 2015Article
- The dual role of iNOS in cancer.Redox biology · 2015Review
- TRAIL-receptor preferences in pancreatic cancer cells revisited: Both TRAIL-R1 and TRAIL-R2 have a licence to kill.BMC cancer · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
We have previously demonstrated that nitrosylcobalamin (NO-Cbl), an analogue of vitamin B12 that delivers nitric oxide (NO), had potent antiproliferative activity against several human cancer cell lines. NO-Cbl induced apoptosis via a death receptor/caspase-8 pathway. In this study, we demonstrate that a functional Apo2L/TRAIL receptor was necessary for the induction of cell death by NO-Cbl. Furthermore, the Apo2L/TRAIL death receptor DR4 (TRAIL R1) was S nitrosylated following NO-Cbl treatment. Human melanoma (A375), renal carcinoma (ACHN), and ovarian carcinoma (NIH-OVCAR-3) cells were treated with NO-Cbl and subjected to the biotin switch assay; S-nitrosylated DR4 was detected in all three cell lines. NO-Cbl treatment did not cause S nitrosylation of DR5. The seven cysteine residues located in the cytoplasmic domain of DR4 were individually point mutated to alanines. NIH-OVCAR-3 cells expressing the DR4 C336A mutation lacked S nitrosylation following NO-Cbl treatment. Overexpression of wild-type DR4 sensitized cells to growth inhibition by NO-Cbl. Cells expressing the DR4 C336A mutant were more resistant to NO-Cbl and Apo2L/TRAIL than were the other six C-A mutations or wild-type cells. The C336A mutant also displayed blunted caspase-8 enzymatic activity following NO-Cbl treatment compared to the other mutants. Thus, DR4 residue C336 becomes S nitrosylated and promotes apoptosis following NO-Cbl treatment.
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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.