ArticleMembranes2022
Interaction of Bortezomib with Cell Membranes Regulates Its Toxicity and Resistance to Therapy.
Article in Membranes, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
4 citing papers in PubMed, 6 citations in OpenAlex.
- Sirt3 deficiency impairs AMPK-Acc1 antilipogenic signaling in female adipocytes.Molecular biology reports · 2026Article
- Transferrin-Conjugated PLGA Nanoparticles for Co-Delivery of Temozolomide and Bortezomib to Glioblastoma Cells.ACS applied nano materials · 2023Article
- Effects of Hydrophobic Gold Nanoparticles on Structure and Fluidity of SOPC Lipid Membranes.International journal of molecular sciences · 2023Article
- In situ Electrochemical Evaluation of the Interaction of dsDNA with the Proteasome Inhibitor Anticancer Drug Bortezomib.Molecules (Basel, Switzerland) · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Bortezomib (BTZ) is a potent proteasome inhibitor currently being used to treat multiple myeloma. However, its high toxicity and resistance to therapy severely limit the treatment outcomes. Drug-membrane interactions have a crucial role in drugs' behavior in vivo, affecting their bioavailability and pharmacological activity. Additionally, drugs' toxicity often occurs due to their effects on the cell membranes. Therefore, studying BTZ's interactions with cell membranes may explain the limitations of its therapy. Due to the cell membranes' complexity, lipid vesicles were proposed here as biomembrane models, focusing on the membrane's main constituents. Two models with distinct composition and complexity were used, one composed of 1,2-dimyristoyl-sn-glycero-3-phosphocholine (DMPC) and the other containing DMPC, cholesterol (Chol), and sphingomyelin (SM). BTZ's interactions with the models were evaluated regarding the drugs' lipophilicity, preferential location, and effects on the membrane's physical state. The studies were conducted at different pH values (7.4 and 6.5) to mimic the normal blood circulation and the intestinal environment, respectively. BTZ revealed a high affinity for the membranes, which proved to be dependent on the drug-ionization state and the membrane complexity. Furthermore, BTZ's interactions with the cell membranes was proven to induce changes in the membrane fluidity. This may be associated with its resistance to therapy, since the activity of efflux transmembrane proteins is dependent on the membrane's fluidity.
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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 OpenQuestion graph.