ArticleNucleic acids research2008
Interaction of anthracyclines with iron responsive element mRNAs.
Article in Nucleic acids research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 64 citations in OpenAlex.
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- Interaction of Selected Anthracycline and Tetracycline Chemotherapeutics with Poly(I:C) Molecules.ACS omega · 2025Article
- Evolution of Theories on Doxorubicin-Induced Late Cardiotoxicity-Role of Topoisomerase.International journal of molecular sciences · 2024Review
- Technologies for Targeted RNA Degradation and Induced RNA Decay.Chemical reviews · 2024Review
- The significance of the apelinergic system in doxorubicin-induced cardiotoxicity.Heart failure reviews · 2024Review
- Neutrophil extracellular traps mediate cardiomyocyte ferroptosis via the Hippo-Yap pathway to exacerbate doxorubicin-induced cardiotoxicity.Cellular and molecular life sciences : CMLS · 2024Article
- An update of the molecular mechanisms underlying anthracycline induced cardiotoxicity.Frontiers in pharmacology · 2024Review
- The dual role of ferroptosis in anthracycline-based chemotherapy includes reducing resistance and increasing toxicity.Cell death discovery · 2023Review
- Review
- Cell death regulation in myocardial toxicity induced by antineoplastic drugs.Frontiers in cell and developmental biology · 2023Review
- Targeting RNA structures with small molecules.Nature reviews. Drug discovery · 2022Review
- Relevance of Ferroptosis to Cardiotoxicity Caused by Anthracyclines: Mechanisms to Target Treatments.Frontiers in cardiovascular medicine · 2022Review
- Understanding Anthracycline Cardiotoxicity From Mitochondrial Aspect.Frontiers in pharmacology · 2022Review
- Anthracycline-induced cardiotoxicity: From pathobiology to identification of molecular targets for nuclear imaging.Frontiers in cardiovascular medicine · 2022Review
- Understanding the Protective Role of Exosomes in Doxorubicin-Induced Cardiotoxicity.Oxidative medicine and cellular longevity · 2022Review
- Adjuvant breast cancer treatments cardiotoxicity and modern methods of detection and prevention of cardiac complications.ESC heart failure · 2021Review
- Regulated cell death pathways in doxorubicin-induced cardiotoxicity.Cell death & disease · 2021Review
- Clinical Implications of Inflammation in Acute Myeloid Leukemia.Frontiers in oncology · 2021Review
- A facile adenosine triphosphate-responsive nanoplatform for efficacious therapy of esophageal cancer.Oncology letters · 2020Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Double-stranded sections of mRNA are often inviting sites of interaction for a wide variety of proteins and small molecules. Interactions at these sites can serve to regulate, or disrupt, the homeostasis of the encoded protein products. Such ligand target sites exist as hairpin-loop structures in the mRNAs of several of the proteins involved in iron homeostasis, including ferritin heavy and light chains, and are known as iron responsive elements (IREs). These IREs serve as the main control mechanism for iron metabolism in the cell via their interaction with the iron regulatory proteins (IRPs). Disruption of the IRE/IRP interaction could greatly affect iron metabolism. Here, we report that anthracyclines, a class of clinically useful chemotherapeutic drugs that includes doxorubicin and daunorubicin, specifically interact with the IREs of ferritin heavy and light chains. We characterized this interaction through UV melting, fluorescence quenching and drug-RNA footprinting. Results from footprinting experiments with wild-type and mutant IREs indicate that anthracyclines preferentially bind within the UG wobble pairs flanking an asymmetrically bulged C-residue, a conserved base that is essential for IRE-IRP interaction. Additionally, drug-RNA affinities (apparent K(d)s) in the high nanomolar range were calculated from fluorescence quenching experiments, while UV melting studies revealed shifts in melting temperature (DeltaT(m)) as large as 10 degrees C. This anthracycline-IRE interaction may contribute to the aberration of intracellular iron homeostasis that results from anthracycline exposure.
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Registered trials
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