ArticleOncotarget2016
Dichloroacetate potentiates tamoxifen-induced cell death in breast cancer cells via downregulation of the epidermal growth factor receptor.
Article in Oncotarget, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- Dichloroacetate for Cancer Treatment: Some Facts and Many Doubts.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Isotope tracing reveals distinct substrate preference in murine melanoma subtypes with differing anti-tumor immunity.Cancer & metabolism · 2022Article
- Review
- Relationship between metabolic reprogramming and drug resistance in breast cancer.Frontiers in oncology · 2022Review
- Impact of Sodium Dichloroacetate Alone and in Combination Therapies on Lung Tumor Growth and Metastasis.International journal of molecular sciences · 2021Article
- Baicalein resensitizes tamoxifen-resistant breast cancer cells by reducing aerobic glycolysis and reversing mitochondrial dysfunction via inhibition of hypoxia-inducible factor-1α.Clinical and translational medicine · 2021Article
- Altered glycolysis results in drug-resistant in clinical tumor therapy.Oncology letters · 2021Review
- Hyperglycemia and Chemoresistance in Breast Cancer: From Cellular Mechanisms to Treatment Response.Frontiers in oncology · 2021Review
- Targeting Glucose Metabolism to Overcome Resistance to Anticancer Chemotherapy in Breast Cancer.Cancers · 2020Review
- Progress in the Understanding of the Mechanism of Tamoxifen Resistance in Breast Cancer.Frontiers in pharmacology · 2020Review
- Inhibition of HIF1α and PDK Induces Cell Death of Glioblastoma Multiforme.Experimental neurobiology · 2017Article
- Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic reprogramming in cancer cells has recently been recognized as an essential hallmark of neoplasia. In this context, metabolic alterations represent an attractive therapeutic target, and encouraging results with drugs targeting various metabolic processes have been obtained in preclinical studies. Recently, several studies have suggested that dichloroacetate (DCA), a specific pyruvate dehydrogenase kinase inhibitor, may be a potential anticancer drug in a large number of diverse tumors. However, the precise mechanism is not fully understood, which is important for the use of DCA in cancer treatment. In the present study, we found that DCA sensitized MCF7 breast cancer cells to tamoxifen-induced cell death by decreasing epidermal growth factor receptor (EGFR) expression. The downregulation of EGFR was caused by degradation of the protein. Furthermore, p38 mitogen-activated protein kinase played an important role in DCA/tamoxifen-induced EGFR degradation. Finally, DCA also promoted comparable tamoxifen-induced cell death in tamoxifen-resistant MCF7 cells, which were established by long-term treatment with tamoxifen. In summary, our results suggest that DCA is an attractive potential drug that sensitizes cells to tamoxifen-induced cell death and overcome tamoxifen resistance via downregulation of EGFR expression in breast cancer cells.
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