ArticleScientific reports2018
FR58P1a; a new uncoupler of OXPHOS that inhibits migration in triple-negative breast cancer cells via Sirt1/AMPK/β1-integrin pathway.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
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Who cites it
46 citing papers in PubMed, 62 citations in OpenAlex.
- Design and Evaluation of Novel Peptides Targeting Protein Disulfide Isomerase as Antiplatelet Agents.Molecules (Basel, Switzerland) · 2026Article
- All the Way: A Decade of SIRT1 in Breast Cancer.Biomedicines · 2026Review
- The role of transmembrane proton transport rates in mild mitochondrial uncoupling by arylamide substituted fatty acids.Chemical science · 2026Article
- The multifaceted roles of mitochondria and their therapeutic transformation: a new perspective on triple-negative breast cancer treatment.Frontiers in oncology · 2026Article
- Review
- SMAP3-ID for Identification of Endogenous Protein-Protein Interactions Reveals Regulation of Mitochondrial Activity by Lamins.JACS Au · 2025Article
- RFX5 promotes the growth, motility, and inhibits apoptosis of gastric adenocarcinoma cells through the SIRT1/AMPK axis.Open life sciences · 2025Article
- The IPBiochimica et biophysica acta. Molecular basis of disease · 2025Article
- The bioenergetic landscape of cancer.Molecular metabolism · 2024Review
- Identification of Antioxidant Methyl Derivatives ofInternational journal of molecular sciences · 2024Article
- Structural investigations on the mitochondrial uncouplers niclosamide and FCCP.FEBS open bio · 2024Article
- CCL2 and Lactate from Chemotherapeutics-Treated Fibroblasts Drive Malignant Traits by Metabolic Rewiring in Low-Migrating Breast Cancer Cell Lines.Antioxidants (Basel, Switzerland) · 2024Article
- Mitochondrial division inhibitor (mdivi-1) induces extracellular matrix (ECM)-detachment of viable breast cancer cells by a DRP1-independent mechanism.Scientific reports · 2024Article
- Targeting Mitochondria for Cancer Treatment.Pharmaceutics · 2024Review
- Metabolic transitions regulate global protein fatty acylation.The Journal of biological chemistry · 2024Article
- A review of biological targets and therapeutic approaches in the management of triple-negative breast cancer.Journal of advanced research · 2023Review
- Noncoupled Mitochondrial Respiration as Therapeutic Approach for the Treatment of Metabolic Diseases: Focus on Transgenic Animal Models.International journal of molecular sciences · 2023Review
- A New Quinone-Based Inhibitor of Mitochondrial Complex I in D-Conformation, Producing Invasion Reduction and Sensitization to Venetoclax in Breast Cancer Cells.Antioxidants (Basel, Switzerland) · 2023Article
- Absence of TRIC-B from type XIV Osteogenesis Imperfecta osteoblasts alters cell adhesion and mitochondrial function - A multi-omics study.Matrix biology : journal of the International Society for Matrix Biology · 2023Article
- Pictolysin-III, a Hemorrhagic Type-III Metalloproteinase Isolated fromPharmaceutics · 2023Article
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Authors and funding
21 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Highly malignant triple-negative breast cancer (TNBC) cells rely mostly on glycolysis to maintain cellular homeostasis; however, mitochondria are still required for migration and metastasis. Taking advantage of the metabolic flexibility of TNBC MDA-MB-231 cells to generate subpopulations with glycolytic or oxidative phenotypes, we screened phenolic compounds containing an ortho-carbonyl group with mitochondrial activity and identified a bromoalkyl-ester of hydroquinone named FR58P1a, as a mitochondrial metabolism-affecting compound that uncouples OXPHOS through a protonophoric mechanism. In contrast to well-known protonophore uncoupler FCCP, FR58P1a does not depolarize the plasma membrane and its effect on the mitochondrial membrane potential and bioenergetics is moderate suggesting a mild uncoupling of OXPHOS. FR58P1a activates AMPK in a Sirt1-dependent fashion. Although the activation of Sirt1/AMPK axis by FR58P1a has a cyto-protective role, selectively inhibits fibronectin-dependent adhesion and migration in TNBC cells but not in non-tumoral MCF10A cells by decreasing β1-integrin at the cell surface. Prolonged exposure to FR58P1a triggers a metabolic reprograming in TNBC cells characterized by down-regulation of OXPHOS-related genes that promote cell survival but comprise their ability to migrate. Taken together, our results show that TNBC cell migration is susceptible to mitochondrial alterations induced by small molecules as FR58P1a, which may have therapeutic implications.
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