ArticleScientific reports2022
Combining PEGylated mito-atovaquone with MCT and Krebs cycle redox inhibitors as a potential strategy to abrogate tumor cell proliferation.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Lactate-induced epithelial-mesenchymal transition: a metabolic nexus in pancreatic cancer metastasis.Translational cancer research · 2026Review
- Microbial Metabolism of Levodopa as an Adjunct Therapeutic Target in Parkinson's Disease.Antioxidants (Basel, Switzerland) · 2026Article
- Mitochondria-targeted strategies in tumor immunity.Frontiers in immunology · 2025Review
- Inhibition of OXPHOS induces metabolic rewiring and reduces hypoxia in murine tumor models.Clinical and translational radiation oncology · 2024Article
- Characterizing OXPHOS inhibitor-mediated alleviation of hypoxia using high-throughput live cell-imaging.Cancer & metabolism · 2024Article
- Mitochondria-targeted atovaquone promotes anti-lung cancer immunity by reshaping tumor microenvironment and enhancing energy metabolism of anti-tumor immune cells.Cancer communications (London, England) · 2024Article
- Current Advances on Nanomaterials Interfering with Lactate Metabolism for Tumor Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Review
- Bioenergetic alteration in gastrointestinal cancers: The good, the bad and the ugly.World journal of gastroenterology · 2023Review
- Incorporating a Polyethyleneglycol Linker to Enhance the Hydrophilicity of Mitochondria-Targeted Triphenylphosphonium Constructs.Chembiochem : a European journal of chemical biology · 2023Article
- Antiproliferative effects of mitochondria-targeted N-acetylcysteine and analogs in cancer cells.Scientific reports · 2023Article
- Polyphenolic Boronates Inhibit Tumor Cell Proliferation: Potential Mitigators of Oxidants in the Tumor Microenvironment.Cancers · 2023Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glycolytic and mitochondrial oxidative metabolism, which are two major energy sources in tumors, are potential targets in cancer treatment. Metabolic reprogramming from glycolysis to mitochondrial oxidative metabolism and vice versa is an adaptive strategy with which tumor cells obtain energy to survive and thrive under the compromised conditions of glycolysis and mitochondrial respiration. Developing highly potent, nontoxic, and tumor-selective oxidative phosphorylation (OXPHOS) inhibitors may help advance therapeutic targeting of mitochondrial drugs in cancer. The FDA-approved antimalarial drug atovaquone (ATO), a mitochondrial complex III inhibitor, was repurposed in cancer treatment. Here, we developed a new class of PEGylated mitochondria-targeted ATO (Mito-(PEG)n-ATO). Depending on the PEGylation chain length (n), Mito-PEG-ATO analogs inhibit both mitochondrial complex I- and complex III-induced oxygen consumption in human pancreatic (MiaPaCa-2) and brain (U87MG) cancer cells. Mito-PEG
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