ArticleCell death & disease2022
Flubendazole induces mitochondrial dysfunction and DRP1-mediated mitophagy by targeting EVA1A in breast cancer.
Article in Cell death & disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 52 citations in OpenAlex.
- Berberine Modulates Mitophagy-Related Gene Expression and Suppresses Breast Cancer Cells: A Multi-Omics and Experimental Study.Cell biochemistry and biophysics · 2026Article
- Transcriptional Heterogeneity Underlying Cancer Cell Migration Converges on Shared Regulatory Programs.Genes · 2026Article
- EVA1A-Mediated Signaling Networks in Physiological and Pathological Contexts: Dual Roles in Autophagy and Apoptosis.Cell biochemistry and biophysics · 2026Review
- Crosstalk between mitophagy and breast cancer: mechanisms of action and clinical applications.Journal of cancer research and clinical oncology · 2026Review
- MUL1 suppresses cervical cancer progression by targeting FUNDC1 for ubiquitination and inhibiting DRP1-dependent mitophagy.Journal of molecular histology · 2026Article
- [EVA1A overexpression improves non-alcoholic fatty liver disease in mice by regulating lipid metabolism and promoting lipophagy].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026Article
- The application of nanotechnology in regulating mitochondrial function in tumor microenvironment for cancer therapy.Theranostics · 2026Review
- Molecular mechanism and potential role of mitophagy in breast cancer.Journal of Cancer · 2026Review
- ROS-Drp1-mitophagy feedback loop regulates myogenic differentiation via actin cytoskeleton remodeling-mediated MRTF-A/SRF axis.Redox report : communications in free radical research · 2025Article
- LncRNA small nucleolar RNA host gene 1 (SNHG1) mediates acidic bile salt-induced EMT via the ULK1-Notch1 axis in Barrett's esophagus.Molecular biomedicine · 2025Article
- ER-mitochondria tethering and its signaling: A novel therapeutic target in breast cancer.Molecular therapy. Oncology · 2025Review
- SLC5A3 depletion promotes apoptosis by inducing mitochondrial dysfunction and mitophagy in gemcitabine-resistant pancreatic cancer cells.Cell death & disease · 2025Article
- DRP1: shedding light on the complex nexus of mitochondrial fission and breast cancer.Future oncology (London, England) · 2025Review
- Effects of photobiomodulation in mitochondrial quantity, biogenesis and mitophagy-associated genes in breast cancer cells.Lasers in medical science · 2025Article
- Development and validation of a machine learning-driven mitochondrial gene signature for the diagnosis of breast cancer.Frontiers in immunology · 2025Article
- Role of mitophagy in breast cancer: mitophagy-apoptosis balance and reactive oxygen species play determining role.Frontiers in physiology · 2025Review
- Anticancer role of flubendazole: Effects and molecular mechanisms (Review).Oncology letters · 2024Review
- Targeting selective autophagy and beyond: From underlying mechanisms to potential therapies.Journal of advanced research · 2024Review
- Mitophagy: insights into its signaling molecules, biological functions, and therapeutic potential in breast cancer.Cell death discovery · 2024Review
- CREB1 regulates RECQL4 to inhibit mitophagy and promote esophageal cancer metastasis.Journal of clinical biochemistry and nutrition · 2024Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Breast cancer is still one of the most common malignancies worldwide and remains a major clinical challenge. We previously reported that the anthelmintic drug flubendazole induced autophagy and apoptosis via upregulation of eva-1 homolog A (EVA1A) in triple-negative breast cancer (TNBC) and was repurposed as a novel anti-tumor agent. However, the detailed underlying mechanisms remain unclear and need further investigation. Here, we found that flubendazole impairs the permeability of the mitochondrial outer membrane and mitochondrial function in breast cancer. Meanwhile, flubendazole increased dynamin-related protein (DRP1) expression, leading to the accumulation of PTEN induced putative kinase 1 (PINK1) and subsequent mitochondrial translocation of Parkin, thereby promoting excessive mitophagy. The resultant excessive mitophagy contributed to mitochondrial damage and dysfunction induced by flubendazole, thus inhibiting breast cancer cells proliferation and migration. Moreover, we demonstrated that excessive DRP1-mediated mitophagy played a critical role in response to the anti-tumor effects of EVA1A in breast cancer. Taken together, our results provide new insights into the molecular mechanisms in relation to the anti-tumor activities of flubendazole, and may be conducive to its rational use in potential clinical applications.
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