ArticleOncology letters2021
β-hydroxybutyrate does not alter the effects of glucose deprivation on breast cancer cells.
Article in Oncology letters, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 19 citations in OpenAlex.
- Ketogenic Diet as an Adjuvant in Epithelial Cancers: Mechanisms, Model Systems, and Translational Opportunities.Cancers · 2026Review
- The significance of the ketolytic gene OXCT1 in metabolism, intracellular signaling and disease development.Cellular and molecular life sciences : CMLS · 2026Review
- β-Hydroxybutyrate Inhibits Angiogenesis, Suppresses Non-Small Cell Lung Cancer Growth, and Enhances Gemcitabine Antitumor Activity.International journal of molecular sciences · 2026Article
- β-Hydroxybutyrate elicits divergent metabolic responses between MCF-7 and T47D ER+ breast cancer cells under glucose restriction.bioRxiv : the preprint server for biology · 2026Article
- The Function and Mechanism of OXCT1 in Tumor Progression as a Critical Ketone Body Metabolic Enzyme.Biomolecules · 2025Review
- BRCAGenie: A machine learning-driven 43-gene polygenic risk score model for precision prediction of breast cancer survival.Journal of translational medicine · 2025Article
- Metabolic Regulation of Ferroptosis in Breast Cancer.International journal of molecular sciences · 2025Review
- OXCT1 promotes triple negative breast cancer immune escape via modulating succinylation modification of PGK1.Communications biology · 2025Article
- Pleiotropic Effects of Metformin on the Chemotherapy Response of HPV-Positive Cancer Cells.Journal of medical virology · 2025Article
- Metabolic Reprogramming and Adaption in Breast Cancer Progression and Metastasis.Advances in experimental medicine and biology · 2025Review
- Ketone body, as an emerging modulator of metabolic reprogramming and epigenetics in breast cancer.Iranian journal of basic medical sciences · 2025Review
- The Use of Patient-Derived Organoids in the Study of Molecular Metabolic Adaptation in Breast Cancer.International journal of molecular sciences · 2024Review
- Metabolic alterations and cellular responses to β-Hydroxybutyrate treatment in breast cancer cells.Cancer & metabolism · 2024Article
- Targeting apoptosis and unfolded protein response: the impact of β-hydroxybutyrate in clear cell renal cell carcinoma under glucose-deprived conditions.Molecular biology reports · 2024Article
- Liver Metastatic Breast Cancer: Epidemiology, Dietary Interventions, and Related Metabolism.Nutrients · 2022Review
- Article
- Recent Metabolomics Analysis in Tumor Metabolism Reprogramming.Frontiers in molecular biosciences · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Ketogenic diets have the potential to lower glucose availability to cancer cells. However, the effect that the resulting increase in ketone bodies has on cancer cells is not fully understood. The present study explored the effect of β-hydroxybutyrate (BHB) on glucose-deprived MCF-7 and T47D breast cancer cells. Cell proliferation was decreased in response to lower glucose conditions, which could not be rescued consistently by 10 or 25 mM BHB supplementation. In addition, gene expression levels were altered when cells were glucose deprived. Reducing glucose availability of cancer cells to 225 mg/l for 4 days significantly decreased the expression of 113 genes and increased the expression of 100 genes in MCF-7 breast cancer cells, and significantly decreased the expression of 425 genes and increased the expression of 447 genes in T47D breast cancer cells. Pathway enrichment analysis demonstrated that glucose deprivation decreased activity of the Hippo-Yap cell signaling pathway in MCF-7 breast cancer cells, whereas it increased the expression of genes in the NRF2-pathaway and genes regulating ferroptosis in T47D breast cancer cells. Treatment of glucose-deprived cells with 10 or 25 mM BHB significantly changed the expression of 14 genes in MCF-7 breast cancer cells and 40 genes in T47D breast cancer cells. No significant pathway enrichment was detected when glucose-deprived cells were treated with BHB. Both cell lines expressed the enzymes (OXCT1/2, BDH1 and ACAT1/2) responsible for metabolizing BHB to acetyl-CoA, yet expression of these enzymes was not altered by either glucose deprivation or BHB treatment. In the publicly available The Cancer Genome Atlas (TCGA), increased expression of ketone body-catabolizing enzymes was observed in various types of cancer based on mRNA expression z-scores. Increased expression of BDH1 and ACAT1 significantly decreased overall survival of patients with breast cancer in TCGA studies, while decreased OXCT1 expression non-significantly decreased overall survival. In conclusion, neither MCF-7 nor T47D breast cancer cells were affected by BHB during glucose deprivation; however, screening of tumors for activation of ketone body-metabolizing enzymes may be able to identify patients that will benefit from ketogenic diet interventions.
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