ArticleProceedings of the National Academy of Sciences of the United States of America1995
Disruption of cellular signaling pathways by daunomycin through destabilization of nonlamellar membrane structures.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 108 citations in OpenAlex.
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- Molecular dynamics simulations of heterogeneous cell membranes in response to uniaxial membrane stretches at high loading rates.Scientific reports · 2017Article
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- A biophysical approach to daunorubicin interaction with model membranes: relevance for the drug's biological activity.Journal of the Royal Society, Interface · 2017Article
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- Minerval induces apoptosis in Jurkat and other cancer cells.Journal of cellular and molecular medicine · 2010Article
- Systolic versus diastolic cardiac function variables during epirubicin treatment for breast cancer.The international journal of cardiovascular imaging · 2010Article
- Pivotal role of dihydrofolate reductase knockdown in the anticancer activity of 2-hydroxyoleic acid.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Albeit anthracyclines are widely used in the treatment of solid tumors and leukemias, their mechanism of action has not been elucidated. The present study gives relevant information about the role of nonlamellar membrane structures in signaling pathways, which could explain how anthracyclines can exert their cytocidal action without entering the cell [Tritton, T. R. & Yee, G. (1982) Science 217, 248-250]. The anthracycline daunomycin reduced the formation of the nonlamellar hexagonal (HII) phase (i.e., the hexagonal phase propensity), stabilizing the bilayer structure of the plasma membrane by a direct interaction with membrane phospholipids. As a consequence, various cellular events involved in signal transduction, such as membrane fusion and membrane association of peripheral proteins [e.g., guanine nucleotide-binding regulatory proteins (G proteins and protein kinase C-alpha beta)], where nonlamellar structures (negative intrinsic monolayer curvature strain) are required, were altered by the presence of daunomycin. Functionally, daunomycin also impaired the expression of the high-affinity state of a G protein-coupled receptor (ternary complex for the alpha 2-adrenergic receptor) due to G-protein dissociation from the plasma membrane. In vivo, daunomycin also decreased the levels of membrane-associated G proteins and protein kinase C-alpha beta in the heart. The occurrence of such nonlamellar structures favors the association of these peripheral proteins with the plasma membrane and prevents daunomycin-induced dissociation. These results reveal an important role of the lipid component of the cell membrane in signal transduction and its alteration by anthracyclines.
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