ArticleInternational journal of molecular sciences2024
Mitochondrial Elongation and ROS-Mediated Apoptosis in Prostate Cancer Cells under Therapy with Apalutamide and Complex I Inhibitor.
Article in International journal of molecular sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- MitoQ Triggers Mitochondrial Collapse and Apoptotic Death in Glioblastoma Associated with KATP Channel Expression Changes.Neurochemical research · 2026Article
- Mitochondrial fission genes MTFP1/MTFP2 as predictive biomarkers in prostate cancer: a mendelian randomization study.Discover oncology · 2025Article
- Multi-omics analysis identifies OSGEPL1 as an oncogene in hepatocellular carcinoma.Discover oncology · 2025Article
- DNA replication stress underpins the vulnerability to oxidative phosphorylation inhibition in colorectal cancer.Cell death & disease · 2025Article
- Mitochondrial involvement in PC: improving therapeutic strategies.Frontiers in pharmacology · 2025Review
- Tumor energy metabolism: implications for therapeutic targets.Molecular biomedicine · 2024Review
- mtPCDI: a machine learning-based prognostic model for prostate cancer recurrence.Frontiers in genetics · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Metabolic reprogramming and mitochondrial dynamics are pivotal in prostate cancer (PCa) progression and treatment resistance, making them essential targets for therapeutic intervention. In this study, we investigated the effects of the androgen receptor antagonist apalutamide (ARN) and the mitochondrial electron transport chain complex I inhibitor IACS-010759 (IACS) on the mitochondrial network architecture and dynamics in PCa cells. Treatment with ARN and/or IACS induced significant changes in mitochondrial morphology, particularly elongation, in androgen-sensitive PCa cells. Additionally, ARN and IACS modulated the mitochondrial fission and fusion processes, indicating a convergence of metabolic and androgen-signaling pathways in shaping mitochondrial function. Notably, the combination treatment with ARN and IACS resulted in increased apoptotic cell death and mitochondrial oxidative stress selectively in the androgen-sensitive PCa cells. Our findings highlight the therapeutic potential of targeting mitochondrial metabolism in prostate cancer and emphasize the need for further mechanistic understanding to optimize treatment strategies and improve patient outcomes.
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Registered trials
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