ArticlePloS one2009
Antiproliferative effect of ascorbic acid is associated with the inhibition of genes necessary to cell cycle progression.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 78 citations in OpenAlex.
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- A novel anticancer natural product SP09 selectively targets KRAS-mutant NSCLC through LKB1/AMPK/mTOR modulation: implications for novel therapeutic development.Anti-cancer drugs · 2026Article
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- Ascorbic acid mitigates cadmium-induced stress, and contributes to ionome stabilization in fission yeast.Environmental science and pollution research international · 2021Article
- High-Dose Vitamin C in Advanced-Stage Cancer Patients.Nutrients · 2021Review
- Two Distinct Faces of Vitamin C: AA vs. DHA.Antioxidants (Basel, Switzerland) · 2021Review
- Comparative study of young shoots and the mature red headed cabbage as antioxidant food resources with antiproliferative effect on prostate cancer cells.RSC advances · 2020Article
- Natural products as safeguards against monosodium glutamate-induced toxicity.Iranian journal of basic medical sciences · 2020Review
- High-Dose Vitamin C Tends to Kill Colorectal Cancer with High MALAT1 Expression.Journal of oncology · 2020Article
- Potential Mechanisms of Action for Vitamin C in Cancer: Reviewing the Evidence.Frontiers in physiology · 2018Review
- Intravenous Vitamin C for Cancer Therapy - Identifying the Current Gaps in Our Knowledge.Frontiers in physiology · 2018Review
- Vitamin C in Cancer: A Metabolomics Perspective.Frontiers in physiology · 2018Review
- Genome-wide expression profiling establishes novel modulatory roles of vitamin C in THP-1 human monocytic cell line.BMC genomics · 2017Article
- Ascorbic acid promotes cardiomyogenesis through SMAD1 signaling in differentiating mouse embryonic stem cells.PloS one · 2017Article
- Oxidative Stress: Harms and Benefits for Human Health.Oxidative medicine and cellular longevity · 2017Review
- Vitamin C supplementation modulates gene expression in peripheral blood mononuclear cells specifically upon an inflammatory stimulus: a pilot study in healthy subjects.Genes & nutrition · 2014Article
- Ascorbic acid is a dose-dependent inhibitor of adipocyte differentiation, probably by reducing cAMP pool.Frontiers in cell and developmental biology · 2014Article
- Ascorbate as a co-factor for fe- and 2-oxoglutarate dependent dioxygenases: physiological activity in tumor growth and progression.Frontiers in oncology · 2014Review
- Parenteral ascorbate as a cancer therapeutic: a reassessment based on pharmacokinetics.Antioxidants & redox signaling · 2013Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAscorbic acid (AA), or Vitamin C, is most well known as a nutritional supplement with antioxidant properties. Recently, we demonstrated that high concentrations of AA act on PMP22 gene expression and partially correct the Charcot-Marie-Tooth disease phenotype in a mouse model. This is due to the capacity of AA, but not other antioxidants, to down-modulate cAMP intracellular concentration by a competitive inhibition of the adenylate cyclase enzymatic activity. Because of the critical role of cAMP in intracellular signalling, we decided to explore the possibility that ascorbic acid could modulate the expression of other genes. METHODS AND
findingsUsing human pangenomic microarrays, we found that AA inhibited the expression of two categories of genes necessary for cell cycle progression, tRNA synthetases and translation initiation factor subunits. In in vitro assays, we demonstrated that AA induced the S-phase arrest of proliferative normal and tumor cells. Highest concentrations of AA leaded to necrotic cell death. However, quiescent cells were not susceptible to AA toxicity, suggesting the blockage of protein synthesis was mainly detrimental in metabolically-active cells. Using animal models, we found that high concentrations of AA inhibited tumor progression in nude mice grafted with HT29 cells (derived from human colon carcinoma). Consistently, expression of tRNA synthetases and ieF2 appeared to be specifically decreased in tumors upon AA treatment.
conclusionsAA has an antiproliferative activity, at elevated concentration that could be obtained using IV injection. This activity has been observed in vitro as well in vivo and likely results from the inhibition of expression of genes involved in protein synthesis. Implications for a clinical use in anticancer therapies will be discussed.
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