ArticleThe Journal of biological chemistry2010
Selenium compounds activate early barriers of tumorigenesis.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The trial behind it
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Who cites it
28 citing papers in PubMed, 72 citations in OpenAlex.
- Selenium compounds for cancer prevention and therapy - human clinical trial considerations.Medical review (2021) · 2025Review
- Effect of Selenium and Selenoproteins on Radiation Resistance.Nutrients · 2024Review
- Combination of Selenite and Butyrate Enhances Efficacy Against Colon Cancer by Targeting ASCT2-Mediated Amino Acid Metabolism.Biological trace element research · 2024Article
- Selenium in cancer management: exploring the therapeutic potential.Frontiers in oncology · 2024Review
- Nontoxic Levels of Se-Containing Compounds Increase Survival by Blocking Oxidative and Inflammatory Stresses via Signal Pathways Whereas High Levels of Se Induce Apoptosis.Molecules (Basel, Switzerland) · 2023Review
- Identification of Selenoprotein H Isoforms and Impact of Selenoprotein H Overexpression on Protein But Not mRNA Levels of 2 Other Selenoproteins in 293T Cells.The Journal of nutrition · 2021Article
- Selenite inhibits glutamine metabolism and induces apoptosis by regulating GLS1 protein degradation via APC/C-CDH1 pathway in colorectal cancer cells.Oncotarget · 2017Article
- Current Knowledge on the Importance of Selenium in Food for Living Organisms: A Review.Molecules (Basel, Switzerland) · 2016Review
- Methylseleninic Acid Superactivates p53-Senescence Cancer Progression Barrier in Prostate Lesions of Pten-Knockout Mouse.Cancer prevention research (Philadelphia, Pa.) · 2016Article
- Cancer chemoprevention research with selenium in the post-SELECT era: Promises and challenges.Nutrition and cancer · 2016Review
- Article
- Evasion of anti-growth signaling: A key step in tumorigenesis and potential target for treatment and prophylaxis by natural compounds.Seminars in cancer biology · 2015Review
- Effects of ebselen and N-acetyl cysteine on replicative aging of primary human fibroblast strains.Immunity & ageing : I & A · 2015Article
- Selenoprotein H suppresses cellular senescence through genome maintenance and redox regulation.The Journal of biological chemistry · 2014Article
- Selenium suppresses leukemia through the action of endogenous eicosanoids.Cancer research · 2014Article
- Methylseleninic acid sensitizes Notch3-activated OVCA429 ovarian cancer cells to carboplatin.PloS one · 2014Article
- Methylseleninic acid suppresses pancreatic cancer growth involving multiple pathways.Nutrition and cancer · 2014Article
- Combination of fenretinide and selenite inhibits proliferation and induces apoptosis in ovarian cancer cells.International journal of molecular sciences · 2013Article
- Selenium supranutrition: are the potential benefits of chemoprevention outweighed by the promotion of diabetes and insulin resistance?Nutrients · 2013Review
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Selenium chemoprevention by apoptosis has been well studied, but it is not clear whether selenium can activate early barriers of tumorigenesis, namely senescence and DNA damage response. To test this hypothesis, we treated normal and cancerous cells with a gradient concentration of sodium selenite, methylseleninic acid and methylselenocysteine for 48 h, followed by a recovery of 1-7 days. Here we show that selenium compounds at doses of </=LD(50) can induce cellular senescence, as evidenced by the expression of senescence-associated beta-galactosidase and 5-bromo-2-deoxyuridine incorporation, in normal but not cancerous cells. In response to clastogens, the ataxia telangiectasia mutated (ATM) protein is rapidly activated, which in turn initiates a cascade of DNA damage response. We found that the ATM pathway is activated by the selenium compounds, and the kinase activity is required for the selenium-induced senescence response. Pretreatment of the MRC-5 non-cancerous cells with the antioxidant N-acetylcysteine or 2,2,6,6-tetramethylpiperidine-1-oxyl suppresses the selenium-induced ATM activation and senescence. Taken together, the results suggest a novel role of selenium in the activation of early tumorigenesis barriers specific in non-cancerous cells, whereby selenium induces an ATM-dependent senescence response that depends on reactive oxygen species.
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Registered trials
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.