ArticleNature communications2017
A novel Fer/FerT targeting compound selectively evokes metabolic stress and necrotic death in malignant cells.
Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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The trial behind it
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Who cites it
12 citing papers in PubMed, 24 citations in OpenAlex.
- The Fer Tyrosine Kinase Mediates EGFR Activation in Sperm Capacitation.International journal of molecular sciences · 2025Article
- Exosome- transported FER inhibitor suppresses progression of diffuse large B-cell lymphoma via regulating AJUBA/Hippo axis.NPJ precision oncology · 2025Article
- Spatiotemporal HNature communications · 2025Article
- An overview of pyridazin-3(2Future medicinal chemistry · 2024Review
- Optimization of Novel Pyrido-pyridazinone Derivatives as FER Tyrosine Kinase Inhibitors, Leading to the Potent DS08701581.ACS medicinal chemistry letters · 2024Article
- Fer governs mTORC1 regulating pathways and sustains viability of pancreatic ductal adenocarcinoma cells.Frontiers in oncology · 2024Article
- Fer and FerT: A New Regulatory Link between Sperm and Cancer Cells.International journal of molecular sciences · 2023Review
- Oxidative DNA Damage-induced PARP-1-mediated Autophagic Flux Disruption Contributes to Bupivacaine-induced Neurotoxicity During Pregnancy.Current neuropharmacology · 2023Article
- Loss of Fer Jeopardizes Metabolic Plasticity and Mitochondrial Homeostasis in Lung and Breast Carcinoma Cells.International journal of molecular sciences · 2021Article
- Article
- High-resolution structural analysis shows how different crystallographic environments can induce alternative modes of binding of a phosphotyrosine peptide to the SH2 domain of Fer tyrosine kinase.Protein science : a publication of the Protein Society · 2019Article
- Discovery of Novel Pyrido-pyridazinone Derivatives as FER Tyrosine Kinase Inhibitors with Antitumor Activity.ACS medicinal chemistry letters · 2019Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Disruption of the reprogrammed energy management system of malignant cells is a prioritized goal of targeted cancer therapy. Two regulators of this system are the Fer kinase, and its cancer cell specific variant, FerT, both residing in subcellular compartments including the mitochondrial electron transport chain. Here, we show that a newly developed inhibitor of Fer and FerT, E260, selectively evokes metabolic stress in cancer cells by imposing mitochondrial dysfunction and deformation, and onset of energy-consuming autophagy which decreases the cellular ATP level. Notably, Fer was also found to associate with PARP-1 and E260 disrupted this association thereby leading to PARP-1 activation. The cooperative intervention with these metabolic pathways leads to energy crisis and necrotic death in malignant, but not in normal human cells, and to the suppression of tumors growth in vivo. Thus, E260 is a new anti-cancer agent which imposes metabolic stress and cellular death in cancer cells.The tyrosine-kinases Fer/FerT associate with the mitochondrial electron transport chain in cancer cells supporting their metabolic reprogramming. Here the authors discover a compound that disrupts Fer /FerT activity and selectively induces cell death of cancer cell lines displaying anti-tumor activity in vivo.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.