ArticleEpigenetics & chromatin2019
Hyperinsulinemia promotes aberrant histone acetylation in triple-negative breast cancer.
Article in Epigenetics & chromatin, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 31 citations in OpenAlex.
- Celastrol at the obesity-cancer interface: critical appraisal of molecular mechanisms, preclinical evidence, and translational barriers.Molecular biology reports · 2026Review
- Insulin Resistance as a Systemic Metabolic Risk State for Cancer: Mechanisms, Biomarkers, and Prevention.International journal of molecular sciences · 2026Review
- A sweet danger: the silent link between hyperinsulinemia and gastric cancer.Molecular cancer · 2026Review
- Early Epigenetic and Metabolic Responses to the Adipocyte Secretome Reveal Stress-Adaptive States in Triple-Negative Breast Cancer.bioRxiv : the preprint server for biology · 2026Article
- Insulin receptor expression and its association with hyperinsulinemia in triple negative breast cancer.Journal of the Endocrine Society · 2026Article
- Insulin potentiates lipopolysaccharide-induced IL-6 expression through epigenetic remodeling in adipocytes:Frontiers in immunology · 2026Article
- Interplay between aging and metabolic diseases: from molecular mechanisms to therapeutic horizons.Medical review (2021) · 2025Review
- Breast Cancer Cell Line-Specific Responses to Insulin: Effects on Proliferation and Migration.International journal of molecular sciences · 2025Article
- Article
- Nuclear mTOR Signaling Orchestrates Transcriptional Programs Underlying Cellular Growth and Metabolism.Cells · 2024Review
- Assessing the Link between Diabetic Metabolic Dysregulation and Breast Cancer Progression.International journal of molecular sciences · 2023Article
- ACAT1-mediated METTL3 acetylation inhibits cell migration and invasion in triple negative breast cancer.Genes and immunity · 2023Article
- CircAGO2 promotes colorectal cancer progression by inhibiting heat shock protein family B (small) member 8 via miR-1-3p/retinoblastoma binding protein 4 axis.Functional & integrative genomics · 2023Article
- Acetyl-CoA metabolism in cancer.Nature reviews. Cancer · 2023Review
- Obesity promotes radioresistance through SERPINE1-mediated aggressiveness and DNA repair of triple-negative breast cancer.Cell death & disease · 2023Article
- Insulinemic potential of diet and risk of total and subtypes of breast cancer among US females.The American journal of clinical nutrition · 2022Article
- Metformin counteracts stimulatory effects induced by insulin in primary breast cancer cells.Journal of translational medicine · 2022Article
- Metabolic Regulation of Lysine Acetylation: Implications in Cancer.Sub-cellular biochemistry · 2022Review
- Epigenome-Wide Histone Acetylation Changes in Peripheral Blood Mononuclear Cells in Patients with Type 2 Diabetes and Atherosclerotic Disease.Biomedicines · 2021Article
- The Bidirectional Relationship Between Cancer Epigenetics and Metabolism.Annual review of cancer biology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundHyperinsulinemia, the presence of excess insulin relative to glucose in the blood, is considered to be a poor prognostic indicator for patients with triple-negative breast cancer (TNBC). mTOR, a downstream effector of insulin, enhances mitochondrial biogenesis and activity, thereby increasing acetyl-CoA precursors. Increased acetyl-CoA can, in turn, be utilized by nuclear acetyltransferases for histone acetylation, a critical feature of genome regulation. While signaling pathways downstream of insulin have been established for sometime, the effect of insulin on chromatin remains unclear. We hypothesized that hyperinsulinemia-induced metabolic changes lead to genome-wide changes in histone acetylation in TNBC.
resultsMDA-MB-231 cells were xenografted into hyperinsulinemic and wild-type mice. Tumors in the hyperinsulinemic mice displayed elevated levels of histone acetylation compared to tumors in normal insulin conditions. We show that insulin treatment in vitro leads to global increase in chromatin-associated histone acetylation, in particular at H3K9, through the PI3K/AKT/mTOR pathway. Genome-wide analyses revealed that most promoter regions have an increase in histone acetylation upon insulin treatment. In addition, insulin induces higher levels of reactive oxygen species and DNA damage foci in cells.
conclusionsThese results demonstrate the impact of hyperinsulinemia on altered gene regulation through chromatin and the importance of targeting hyperinsulinemia-induced processes that lead to chromatin dysfunction in TNBC.
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Registered trials
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