ArticleCancer research2010
Disulfiram treatment facilitates phosphoinositide 3-kinase inhibition in human breast cancer cells in vitro and in vivo.
Article in Cancer research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers, 1 of them a synthesis that pooled it.
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Who cites it
55 citing papers in PubMed, 1 synthesis or guideline pooled it, 113 citations in OpenAlex.
- Cuproptosis: Mechanisms, biological significance, and advances in disease treatment-A systematic review.CNS neuroscience & therapeutics · 2024Pooled it
- A novel combination therapy for ER+ breast cancer suppresses drug resistance via an evolutionary double-bind.Molecular systems biology · 2026Article
- Cuproptosis and Diabetic Osteoporosis: Mechanisms and Therapeutic Prospects.International journal of molecular sciences · 2026Review
- Lung cancer chemo-interception by sulfasalazine and disulfiram codelivered using a nano self-emulsifying drug delivery system in mice.Carcinogenesis · 2025Article
- Marine Natural Product Chagosendine C Induces Cuproptosis in Colorectal Cancer Cells by Targeting FDX1.Journal of the American Chemical Society · 2025Article
- Cuproptosis in prostate cancer: Molecular mechanisms, prognostic biomarkers and therapeutic frontiers of cuproptosis‑related genes (Review).International journal of oncology · 2025Review
- Targeting cuproptosis for cancer therapy: Focus on the anti-tumor immune system.Cancer pathogenesis and therapy · 2025Review
- Exploring disulfiram mechanisms in renal fibrosis: insights from biological data and computational approaches.Frontiers in pharmacology · 2025Article
- Cuproptosis: a promising new target for breast cancer therapy.Cancer cell international · 2024Review
- Targeting cuproptosis for cancer therapy: mechanistic insights and clinical perspectives.Journal of hematology & oncology · 2024Review
- Review
- Targeting the initiator to activate both ferroptosis and cuproptosis for breast cancer treatment: progress and possibility for clinical application.Frontiers in pharmacology · 2024Review
- Inhibition of lung adenocarcinoma by combinations of sulfasalazine (SAS) and disulfiram-copper (DSF-Cu) in cell line models and mice.Carcinogenesis · 2023Article
- Systematic pan-cancer analysis identifies SLC31A1 as a biomarker in multiple tumor types.BMC medical genomics · 2023Article
- Disulfiram enhances the antitumor activity of cisplatin by inhibiting the Fanconi anemia repair pathway.Journal of Zhejiang University. Science. B · 2023Article
- Pan-cancer analyses reveal molecular and clinical characteristics of cuproptosis regulators.iMeta · 2023Article
- Copper-related genes predict prognosis and characteristics of breast cancer.Frontiers in immunology · 2023Article
- Copper homeostasis and cuproptosis in health and disease.Signal transduction and targeted therapy · 2022Review
- Cytotoxic effect of disulfiram/copper on human cervical cancer cell lines and LGR5-positive cancer stem-like cells.BMC cancer · 2022Article
- The cuproptosis related genes signature predicts the prognosis and correlates with the immune status of clear cell renal cell carcinoma.Frontiers in genetics · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Frequent genetic alterations of the components in the phosphoinositide 3-kinase (PI3K)/PTEN/AKT signaling pathway contribute greatly to breast cancer initiation and progression, which makes targeting this signaling pathway a promising therapeutic strategy for breast cancer treatment. In this study, we showed that in the presence of copper (Cu), disulfiram (DSF), a clinically used antialcoholism drug, could potently inhibit breast cancer cell growth regardless of the PIK3CA status. Surprisingly, the treatment with a mixture of DSF and copper (DSF-Cu) led to the decreased expression of PTEN protein and the activation of AKT in a dose- and time-dependent manner in different cell lines with or without PIK3CA mutations. Treatment of breast cancer cell lines with a combination of DSF-Cu and LY294002, a pan-PI3K inhibitor, resulted in the significant inhibition of cell growth when compared with either drug alone. In addition, the combined treatment of DSF and LY294002 significantly inhibited the growth of the breast tumor xenograft in nude mice induced by MDA-MB-231 cells expressing mutant PIK3CA-H1047R and PIK3CA-E545K, whereas neither DSF nor LY294002 alone could significantly retard tumor growth. Finally, the observed in vivo inhibitory effects are found associated with aberrant signaling alterations and apoptosis-inducing activities in tumor samples. Thus, our finding shows for the first time that treatment of breast cancer with DSF results in a novel feedback mechanism that activates AKT signaling. Our study also suggests that the combination of DSF and a PI3K inhibitor may offer a new combinational treatment model for breast cancer, particularly for those with PIK3CA mutations.
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Registered trials
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