ArticleCell death & disease2017
Photo-activation of the delocalized lipophilic cation D112 potentiates cancer selective ROS production and apoptosis.
Article in Cell death & disease, 2017. 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.
- Overcoming resistance in lung cancer: combined mitochondrial destabilization by lipophilic cations and doxycycline in hypoxic non-small cell lung carcinoma.Frontiers in pharmacology · 2026Article
- Mitochondrial DNA-targeted therapy: A novel approach to combat cancer.Cell insight · 2023Review
- Interaction of Cyanine-D112 with Binary Lipid Mixtures: Molecular Dynamics Simulation and Differential Scanning Calorimetry Study.ACS omega · 2022Article
- Recent Advancements in Mitochondria-Targeted Nanoparticle Drug Delivery for Cancer Therapy.Nanomaterials (Basel, Switzerland) · 2022Review
- Medicinal Chemistry Targeting Mitochondria: From New Vehicles and Pharmacophore Groups to Old Drugs with Mitochondrial Activity.International journal of molecular sciences · 2020Review
- ROS as a novel indicator to predict anticancer drug efficacy.BMC cancer · 2019Article
- Non-canonical BAD activity regulates breast cancer cell and tumor growth via 14-3-3 binding and mitochondrial metabolism.Oncogene · 2019Article
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Authors and funding
5 authors.
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Abstract
Delocalized lipophilic cations (DLCs) selectively accumulate in cancer cell mitochondria and have long been explored for therapeutic applications. Although targeted effects to cancer cells are demonstrated in vitro, non-specific toxicities in vivo have hampered clinical development. Identifying the molecular mechanisms of action and enhancing selectivity are thus necessary next steps to improve these compounds and evaluate their suitability for further drug development. D112 is one such DLC with promising properties. We previously demonstrated that D112 selectively induced intrinsic apoptosis in transformed versus non-transformed cell lines. Here we show that D112 preferentially entered transformed cells where it interacted with, and damaged mitochondrial DNA, inhibited Complex I respiration and induced reactive oxygen species (ROS). ROS production was critical for Bax activation and subsequent apoptosis. Importantly, photo-activation of D112 potentiated selective ROS production and increased the window of toxicity towards cancer cells over non-transformed cells. Thus photodynamic therapy would be an exciting adjunct to D112 studies and may be generally applicable for other DLCs that are currently under therapeutic investigation.
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