ArticlePloS one2013
Bioenergetic and antiapoptotic properties of mitochondria from cultured human prostate cancer cell lines PC-3, DU145 and LNCaP.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 56 citations in OpenAlex.
- Decoding the metabolic‑immune crosstalk: The role of glutamine and ammonium reprogramming in prostate cancer immune evasion (Review).Oncology reports · 2026Review
- Rethinking Human Energy Metabolism.Current issues in molecular biology · 2026Review
- Imaging the uptake and metabolism of glutamine in prostate tumor models using CEST MRI.Npj imaging · 2025Article
- Effects of Docosahexaenoic Acid on Prostate Cancer.Journal of xenobiotics · 2025Review
- Review
- The polyunsaturated fatty acid docosahexaenoic affects mitochondrial function in prostate cancer cells.Cancer & metabolism · 2024Article
- Metabolic flexibility ensures proper neuronal network function in moderate neuroinflammation.Scientific reports · 2024Article
- Article
- PIM3 Kinase: A Promising Novel Target in Solid Cancers.Cancers · 2024Review
- Identification of TMEM126A as OXA1L-interacting protein reveals cotranslational quality control in mitochondria.Molecular cell · 2024Article
- Mitochondrial Redox Balance of Fibroblasts Exposed to Ti-6Al-4V Microplates Subjected to Different Types of Anodizing.International journal of molecular sciences · 2023Article
- Immunoproteasome-specific subunit PSMB9 induction is required to regulate cellular proteostasis upon mitochondrial dysfunction.Nature communications · 2023Article
- Sex as Biological Variable in Cardiac Mitochondrial Bioenergetic Responses to Acute Stress.International journal of molecular sciences · 2022Article
- High resolution respirometry of isolated mitochondria from adult Octopus maya (Class: Cephalopoda) systemic heart.PloS one · 2022Article
- Article
- Curcumin and Carnosic Acid Cooperate to Inhibit Proliferation and Alter Mitochondrial Function of Metastatic Prostate Cancer Cells.Antioxidants (Basel, Switzerland) · 2021Article
- Synthetic Retinoids as Potential Therapeutics in Prostate Cancer-An Update of the Last Decade of Research: A Review.International journal of molecular sciences · 2021Review
- MCART1/SLC25A51 is required for mitochondrial NAD transport.Science advances · 2020Article
- Mitochondrial oncobioenergetics of prostate tumorigenesis.Oncology letters · 2019Review
- Albumin-linked prostate-specific antigen-activated thapsigargin- and niclosamide-based molecular grenades targeting the microenvironment in metastatic castration-resistant prostate cancer.Asian journal of urology · 2019Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
The purpose of this work was to reveal the metabolic features of mitochondria that might be essential for inhibition of apoptotic potential in prostate cancer cells. We studied mitochondria isolated from normal prostate epithelial cells (PrEC), metastatic prostate cancer cell lines LNCaP, PC-3, DU145; and non-prostate cancer cells - human fibrosarcoma HT1080 cells; and normal human lymphoblastoid cells. PrEC cells contained 2 to 4 times less mitochondria per gram of cells than the three PC cell lines. Respiratory activities of PrEC cell mitochondria were 5-20-fold lower than PC mitochondria, depending on substrates and the metabolic state, due to lower content and lower activity of the respiratory enzyme complexes. Mitochondria from the three metastatic prostate cancer cell lines revealed several features that are distinctive only to these cells: low affinity of Complex I for NADH, 20-30 mV higher electrical membrane potential (ΔΨ). Unprotected with cyclosporine A (CsA) the PC-3 mitochondria required 4 times more Ca²⁺ to open the permeability transition pore (mPTP) when compared with the PrEC mitochondria, and they did not undergo swelling even in the presence of alamethicin, a large pore forming antibiotic. In the presence of CsA, the PC-3 mitochondria did not open spontaneously the mPTP. We conclude that the low apoptotic potential of the metastatic PC cells may arise from inhibition of the Ca²⁺-dependent permeability transition due to a very high ΔΨ and higher capacity to sequester Ca²⁺. We suggest that due to the high ΔΨ, mitochondrial metabolism of the metastatic prostate cancer cells is predominantly based on utilization of glutamate and glutamine, which may promote development of cachexia.
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Registered trials
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