ArticleProceedings of the National Academy of Sciences of the United States of America2001
Nitric oxide-induced cytostasis and cell cycle arrest of a human breast cancer cell line (MDA-MB-231): potential role of cyclin D1.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 176 citations in OpenAlex.
- Spatiotemporal Nitric Oxide Modulation via Electrochemical Platform to Profile Tumor Cell Response.Angewandte Chemie (International ed. in English) · 2024Article
- Identification of small molecular inhibitors of SIRT3 by computational and biochemical approaches a potential target of breast cancer.Scientific reports · 2024Article
- Arsenic Trioxide Suppresses Angiogenesis in Non-small Cell Lung CancerAnti-cancer agents in medicinal chemistry · 2024Article
- Understanding the Clinical Use of Levosimendan and Perspectives on its Future in Oncology.Biomolecules · 2023Review
- Repurposing of the Drug Tezosentan for Cancer Therapy.Current issues in molecular biology · 2023Review
- Roles of Regulatory T Cell-Derived Extracellular Vesicles in Human Diseases.International journal of molecular sciences · 2022Review
- Gasotransmitters in the tumor microenvironment: Impacts on cancer chemotherapy (Review).Molecular medicine reports · 2022Review
- Anticancer Impact of Nitric Oxide (NO) and NO Combination with SMYD-3 Inhibitor on Breast Carcinomas.Diseases (Basel, Switzerland) · 2021Article
- Statins' Regulation of the Virulence Factors ofAntioxidants (Basel, Switzerland) · 2021Review
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- Synergism of TNF-α and IFN-γ triggers inflammatory cell death, tissue damage, and mortality in SARS-CoV-2 infection and cytokine shock syndromes.bioRxiv : the preprint server for biology · 2020Article
- Nitric Oxide in the Control of theFrontiers in cell and developmental biology · 2020Article
- Nitric Oxide and S-Nitrosylation in Cancers: Emphasis on Breast Cancer.Breast cancer : basic and clinical research · 2020Review
- Iron-Sulfur Cluster Repair Contributes to Yersinia pseudotuberculosis Survival within Deep Tissues.Infection and immunity · 2019Article
- Sp1-regulated expression of p11 contributes to motor neuron degeneration by membrane insertion of TASK1.Nature communications · 2019Article
- Temporal inhibition of mouse mammary gland cancer metastasis by CORM-A1 and DETA/NO combination therapy.Theranostics · 2019Article
- Extracellular vesicles derived from T regulatory cells suppress T cell proliferation and prolong allograft survival.Scientific reports · 2017Article
- Systemic RALA/iNOS Nanoparticles: A Potent Gene Therapy for Metastatic Breast Cancer Coupled as a Biomarker of Treatment.Molecular therapy. Nucleic acids · 2017Article
- Increased sensitivity of African American triple negative breast cancer cells to nitric oxide-induced mitochondria-mediated apoptosis.BMC cancer · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
DETA-NONOate, a nitric oxide (NO) donor, induced cytostasis in the human breast cancer cells MDA-MB-231, and the cells were arrested in the G(1) phase of the cell cycle. This cytostatic effect of the NO donor was associated with the down-regulation of cyclin D1 and hypophosphorylation of the retinoblastoma protein. No changes in the levels of cyclin E or the catalytic partners of these cyclins, CDK2, CDK4, or CDK6, were observed. This NO-induced cytostasis and decrease in cyclin D1 was reversible for up to 48 h of DETA-NONOate (1 mM) treatment. DETA-NONOate (1 mM) produced a steady-state concentration of 0.5 microM of NO over a 24-h period. Synchronized population of the cells exposed to DETA-NONOate remained arrested at the G(1) phase of the cell cycle whereas untreated control cells progressed through the cell cycle after serum stimulation. The cells arrested at the G(1) phase after exposure to the NO donor had low cyclin D1 levels compared with the control cells. The levels of cyclin E and CDK4, however, were similar to the control cells. The decline in cyclin D1 protein preceded the decrease of its mRNA. This decline of cyclin D1 was due to a decrease in its synthesis induced by the NO donor and not due to an increase in its degradation. We conclude that down-regulation of cyclin D1 protein by DETA-NONOate played an important role in the cytostasis and arrest of these tumor cells in the G(1) phase of the cell cycle.
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