ArticleBritish journal of cancer2025
Repurposing chlorpromazine for the treatment of triple-negative breast cancer growth and metastasis based on modulation of mitochondria-mediated apoptosis and autophagy/mitophagy.
Article in British journal of cancer, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Decoding Mitophagy in Breast Cancer: Biological Mechanisms, Dual Roles, and Clinical Implications.Cells · 2026Review
- Multi-omics analyses related to mitochondria and ageing in triple-negative breast cancer implicate PYCR1 potentiates tumor progression.Cancer cell international · 2026Article
- Molecular mechanism and potential role of mitophagy in breast cancer.Journal of Cancer · 2026Review
- Unlocking Novel Therapeutic Potential of Angiotensin II Receptor Blockers.International journal of molecular sciences · 2025Review
- Role of mitophagy in breast cancer: mitophagy-apoptosis balance and reactive oxygen species play determining role.Frontiers in physiology · 2025Review
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Authors and funding
9 authors.
Funding
Abstract
backgroundTriple-negative breast cancer (TNBC) presents significant challenges due to its aggressive nature and high propensity for brain metastasis, often exhibiting resistance to standard treatments. In this study, we conducted a preliminary screening of potential therapeutic agents and identified chlorpromazine (CPZ) as a promising candidate for treating TNBC and its brain metastases.
methodsThe inhibitory activities of CPZ and its combination with several standard treatment drugs were evaluated in preclinical TNBC models. The mechanism of CPZ on TNBC was elucidated using TMT-labeled quantitative proteomics analysis.
resultsIn vivo experiments demonstrated that CPZ robustly suppressed tumor growth and metastasis, particularly in lung and brain models. Importantly, CPZ enhanced the efficacy of standard therapeutic agents such as vinorelbine (NVB) and anti-PD-1 antibody. Mechanistically, CPZ induced G2/M phase arrest and triggered mitochondria-mediated intrinsic apoptosis in TNBC cells. Furthermore, CPZ triggered incomplete autophagy and activated PINK1-Parkin-mediated mitophagy. Inhibiting autophagy/mitophagy augmented CPZ's anticancer effects, indicating these processes may have cell protective roles.
conclusionsOur study highlights the dual function of CPZ in suppressing TNBC growth and metastasis, positioning it as a promising candidate for treating this aggressive cancer. Additionally, targeting autophagy/mitophagy may serve as an effective strategy to enhance anticancer therapies against TNBC.
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