ArticleOncotarget2015
Enhancement of NAD⁺-dependent SIRT1 deacetylase activity by methylselenocysteine resets the circadian clock in carcinogen-treated mammary epithelial cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- Proteomic Identification of PFKFB3 and PFKFB4 Associated with Coenzyme Metabolism and Redox Imbalance in Dairy Cows with Clinical Mastitis.Antioxidants (Basel, Switzerland) · 2026Article
- Combined use of multiparametric high-content-screening and in vitro circadian reporter assays in neurotoxicity evaluation.Archives of toxicology · 2024Article
- Increased SIRT1 Concentration Following Four Years of Selenium and QAntioxidants (Basel, Switzerland) · 2023Article
- The impacts of resveratrol on the retinal degeneration in a rat model of retinitis pigmentosa induced by alkylation: an in-vivo study.Animal cells and systems · 2023Article
- Circadian Effects of Drug Responses.Annual review of biomedical engineering · 2021Article
- Pathway-level analysis of genome-wide circadian dynamics in diverse tissues in rat and mouse.Journal of pharmacokinetics and pharmacodynamics · 2021Article
- Gene therapy-emulating small molecule treatments in cystic fibrosis airway epithelial cells and patients.Respiratory research · 2019Article
- The emerging link between cancer, metabolism, and circadian rhythms.Nature medicine · 2018Review
- Correlations between SIRT1 gene polymorphisms and diabetic kidney disease.Royal Society open science · 2018Article
- In Vitro Bioluminescence Assay to Characterize Circadian Rhythm in Mammary Epithelial Cells.Journal of visualized experiments : JoVE · 2017Article
- Uncoupling genotoxic stress responses from circadian control increases susceptibility to mammary carcinogenesis.Oncotarget · 2017Article
- The reason for the amelioration of N-methyl-N-nitrosourea-induced retinitis pigmentosa in rats by hydrogen-rich saline.International journal of ophthalmology · 2017Article
- The Synergistic Role of Light-Feeding Phase Relations on Entraining Robust Circadian Rhythms in the Periphery.Gene regulation and systems biology · 2017Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
We previously reported that dietary methylselenocysteine (MSC) inhibits N-methyl-N-nitrosourea (NMU)-induced mammary tumorigenesis by resetting circadian gene expression disrupted by the carcinogen at the early stage of tumorigenesis. To investigate the underlying mechanism, we developed a circadian reporter system comprised of human mammary epithelial cells with a luciferase reporter driven by the promoter of human PERIOD 2 (PER2), a core circadian gene. In this in vitro model, NMU disrupted cellular circadian rhythm in a pattern similar to that observed with SIRT1-specific inhibitors; in contrast, MSC restored the circadian rhythms disrupted by NMU and protected against SIRT1 inhibitors. Moreover, NMU inhibited intracellular NAD+/NADH ratio and reduced NAD+-dependent SIRT1 activity in a dose-dependent manner, while MSC restored NAD+/NADH and SIRT1 activity in the NMU-treated cells, indicating that the NAD+-SIRT1 pathway was targeted by NMU and MSC. In rat mammary tissue, a carcinogenic dose of NMU also disrupted NAD+/NADH oscillations and decreased SIRT1 activity; dietary MSC restored NAD+/NADH oscillations and increased SIRT1 activity in the mammary glands of NMU-treated rats. MSC-induced SIRT1 activity was correlated with decreased acetylation of BMAL1 and increased acetylation of histone 3 lysine 9 at the Per2 promoter E-Box in mammary tissue. Changes in SIRT1 activity were temporally correlated with loss or restoration of rhythmic Per2 mRNA expression in NMU-treated or MSC-rescued rat mammary glands, respectively. Together with our previous findings, these results suggest that enhancement of NAD+-dependent SIRT1 activity contributes to the chemopreventive efficacy of MSC by restoring epigenetic regulation of circadian gene expression at early stages of mammary tumorigenesis.
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