ArticleScientific reports2021
Stress hormones promote DNA damage in human oral keratinocytes.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 25 citations in OpenAlex.
- A Remote Time-Restricted Eating and Mindfulness Intervention Addressing Risk Factors Associated with Early-Onset Colorectal Cancer Demonstrates Feasibility and Acceptability among Young Adults: A Randomized Controlled Pilot Trial.Nutrition and cancer · 2025Trial
- Gut-Brain-Skin Axis: From Mechanistic Insights to Translational Applications in Neurocosmetics.Dermatology and therapy · 2026Review
- Stress regulatory hormones and cancer: the contribution of epinephrine and cancer therapeutic value of beta blockers.Endocrine · 2025Review
- Potential non-invasive biomarkers of chronic sleep disorders identified by salivary metabolomic profiling among middle-aged Japanese men.Scientific reports · 2025Article
- Cancer neuroscience in head and neck: interactions, modulation, and therapeutic strategies.Molecular cancer · 2025Review
- Oral cancer cells secrete stress neurotransmitter and proliferate in response to tobacco carcinogen NNK.Endocrine oncology (Bristol, England) · 2025Article
- Activation of the sympathetic-adrenal-medullary system increases DNA damage during the transition to captivity.Integrative organismal biology (Oxford, England) · 2025Article
- Epinephrine as a potential driver of oral lichen planus pathogenesis.Animal cells and systems · 2025Article
- Stress Hormones: Unveiling the Role in Accelerated Cellular Senescence.Aging and disease · 2024Review
- Review
- Understanding the role of nerves in head and neck cancers - a review.Oncology reviews · 2024Review
- Feline Uroepithelial Cell Culture as a Novel Model of Idiopathic Cystitis: Investigations on the Effects of Norepinephrine on Inflammatory Response, Oxidative Stress, and Barrier Function.Veterinary sciences · 2023Article
- Review
- Investigating the crosstalk between chronic stress and immune cells: implications for enhanced cancer therapy.Frontiers in neuroscience · 2023Review
- Wip1 contributes to the adaptation of HepG2 human liver cancer cells to stress hormone-induced DNA damage.Oncology letters · 2023Article
- Interplay between stress and cancer-A focus on inflammation.Frontiers in physiology · 2023Review
- Psychological distress and eustress in cancer and cancer treatment: Advances and perspectives.Science advances · 2022Review
- Predisposing factors for increased cortisol levels in oral cancer patients.Comprehensive psychoneuroendocrinology · 2022Article
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic stress increases the systemic levels of stress hormones norepinephrine and cortisol. As well as tobacco-specific carcinogen NNK (4-(methylnitrosamine)-1-(3-pyridyl)-1-butanone), they can induce expressive DNA damage contributing to the cancer development. However, it is unknown whether stress hormones have genotoxic effects in oral keratinocytes. This study investigated the effects of stress hormones on DNA damage in a human oral keratinocyte cell line (NOK-SI). NOK-SI cells stimulated with norepinephrine or cortisol showed higher DNA damage compared to untreated cells. Norepinephrine-induced DNA damage was reversed by pre-treatment with beta-adrenergic blocker propranolol. Cells treated with NNK combined to norepinephrine displayed reduced levels of caspases 3 and 7. Cortisol also reduced the activity of pro-apoptotic enzymes. NNK or norepinephrine promoted single-strand breaks and alkali-label side breaks in the DNA of NOK-SI cells. Pre-treatment of cells with propranolol abolished these effects. Carcinogen NNK in the presence or absence of cortisol also induced DNA damage of these cells. The genotoxic effects of cortisol alone and hormone combined with NNK were blocked partially and totally, respectively, by the glucocorticoid receptor antagonist RU486. DNA damage promoted by NNK or cortisol and carcinogen combined to the hormone led to intracellular γH2AX accumulation. The effects caused by NNK and cortisol were reversed by propranolol and glucocorticoid receptor antagonist RU486, respectively. Propranolol inhibited the oxidation of basis induced by NNK in the presence of DNA-formamidopyrimidine glycosylase. DNA breaks induced by norepinephrine in the presence or absence of NNK resulted in higher 8OHdG cellular levels. This effect was also induced through beta-adrenergic receptors. Together, these findings indicate that stress hormones induce DNA damage of oral keratinocytes and could contribute to oral carcinogenesis.
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