ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2012
Epigenetic changes induced by oxidative stress in colorectal cancer cells: methylation of tumor suppressor RUNX3.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 114 citations in OpenAlex.
- Epigenetic regulation of ferroptosis in gastrointestinal cancers (Review).International journal of molecular medicine · 2025Review
- TAS2R38 gene methylation is associated with syndrome Coronavirus 2 (SARS-CoV-2) infection and clinical symptoms.Scientific reports · 2025Article
- Reduced murine double minute-2 methylation from peripheral blood mononuclear cells correlates with enhanced oxidative stress in hepatitis b virus-related hepatocellular carcinoma.Frontiers in microbiology · 2025Article
- Exposure to a Titanium Dioxide Product Alters DNA Methylation in Human Cells.Nanomaterials (Basel, Switzerland) · 2024Article
- Oxidative Stress-Mediated RUNX3 Mislocalization Occurs Via Jun Activation Domain-Binding Protein 1 and Histone Modification.Applied biochemistry and biotechnology · 2024Article
- An Adverse Outcome Pathway Network for Chemically Induced Oxidative Stress Leading to (Non)genotoxic Carcinogenesis.Chemical research in toxicology · 2023Review
- Review
- Mitochondrial Control in Inflammatory Gastrointestinal Diseases.International journal of molecular sciences · 2022Review
- An Epigenetic Role of Mitochondria in Cancer.Cells · 2022Review
- Redox Homeostasis in Thyroid Cancer: Implications in NaInternational journal of molecular sciences · 2022Review
- Epigenetics of Dendritic Cells in Tumor Immunology.Cancers · 2022Review
- Stress Responses as Master Keys to Epigenomic Changes in Transcriptome and Metabolome for Cancer Etiology and Therapeutics.Molecular and cellular biology · 2022Article
- Article
- Identification of Novel MeCP2 Cancer-Associated Target Genes and Post-Translational Modifications.Frontiers in oncology · 2020Article
- Runx3 expression in rectal cancer cells and its effect on cell invasion and proliferation.Oncology letters · 2019Article
- ROS promote epigenetic remodeling and cardiac dysfunction in offspring following maternal engineered nanomaterial (ENM) exposure.Particle and fibre toxicology · 2019Article
- Emerging Perspective: Role of Increased ROS and Redox Imbalance in Skin Carcinogenesis.Oxidative medicine and cellular longevity · 2019Review
- Hints on ATGL implications in cancer: beyond bioenergetic clues.Cell death & disease · 2018Review
- Mitochondrial DNA variants in colorectal carcinogenesis: Drivers or passengers?Journal of cancer research and clinical oncology · 2017Review
- Transient and permanent changes in DNA methylation patterns in inorganic arsenic-mediated epithelial-to-mesenchymal transition.Toxicology and applied pharmacology · 2017Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Runt domain transcription factor 3 (RUNX3) is a tumor suppressor that is silenced in cancer via hypermethylation of its promoter. This study investigated the mechanisms involved in reactive oxygen species (ROS)-induced silencing of RUNX3 in terms of epigenetic alteration since the effects of oxidative stress in tumor suppressor gene transcription are largely unknown. RUNX3 mRNA and protein expressions were down-regulated in response to hydrogen peroxide (H(2)O(2)) in the human colorectal cancer cell line SNU-407. This down-regulation was abolished with pretreatment of the ROS scavenger, N-acetylcysteine (NAC). Moreover, methylation-specific PCR data revealed that H(2)O(2) treatment increased RUNX3 promoter methylation; however, NAC and the cytosine methylation inhibitor, 5-aza-2-deoxycytidine (5-Aza-dC), decreased it, suggesting that an epigenetic regulatory mechanism by ROS-induced methylation may be involved in RUNX3 silencing. H(2)O(2) treatment resulted in DNA methyltransferase 1 (DNMT1) and histone deacetylase 1 (HDAC1) up-regulation with increased expression and activity, increased binding of DNMT1 to HADC1, and increased DNMT1 binding to the RUNX3 promoter. In addition, 5-Aza-dC treatment prevented the decrease in RUNX3 mRNA and protein levels by H(2)O(2) treatment. Additionally, H(2)O(2) treatment inhibited the nuclear localization and expression of RUNX3, which was abolished by NAC treatment. Furthermore, the down-regulation of RUNX3 expression by H(2)O(2) also influenced cell proliferation. Taken together, the data suggested that ROS silenced the tumor suppressor, RUNX3, by epigenetic regulation and may therefore be associated with the progression of colorectal cancer.
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