ArticleScientific reports2019
Methyl-β-cyclodextrin, an actin depolymerizer augments the antiproliferative potential of microtubule-targeting agents.
Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 27 citations in OpenAlex.
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- APP and Bace1: Differential effect of cholesterol enrichment on processing and plasma membrane mobility.iScience · 2023Article
- 4D Force Detection of Cell Adhesion and Contractility.Nano letters · 2023Article
- Phosphomevalonate Kinase Controls β-Catenin Signaling via the Metabolite 5-Diphosphomevalonate.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Scalable large-area mesh-structured microfluidic gradient generator for drug testing applications.Biomicrofluidics · 2022Article
- Membrane Cholesterol Is a Critical Determinant for Hippocampal Neuronal Polarity.Frontiers in molecular neuroscience · 2021Article
- ELAVL1 Role in Cell Fusion and Tunneling Membrane Nanotube Formations with Implication to Treat Glioma Heterogeneity.Cancers · 2020Review
- Direct Regulation of the T Cell Antigen Receptor's Activity by Cholesterol.Frontiers in cell and developmental biology · 2020Review
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3 authors at 1 institution in 1 country.
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Abstract
Methyl-β-cyclodextrin (MCD), an established pharmacological excipient, depolymerizes the actin cytoskeleton. In this work, we investigated the effect of MCD-mediated actin depolymerization on various cellular phenotypes including traction force, cell stiffness, focal adhesions, and intracellular drug accumulation. In addition to a reduction in the contractile cellular traction, MCD acutely inhibits the maturation of focal adhesions. Alteration of contractile forces and focal adhesions affects the trypsin-mediated detachment kinetics of cells. Moreover, MCD-mediated actin depolymerization increases the intracellular accumulation of microtubule-targeting agents (MTAs) by ~50% with respect to the untreated cells. As MCD treatment enhances the intracellular concentration of drugs, we hypothesized that the MCD-sensitized cancer cells could be effectively killed by low doses of MTAs. Our results in cervical, breast, hepatocellular, prostate cancer and multidrug-resistant breast cancer cells confirmed the above hypothesis. Further, the combined use of MCD and MTAs synergistically inhibits the proliferation of tumor cells. These results indicate the potential use of MCD in combination with MTAs for cancer chemotherapy and suggest that targeting both actin and microtubules simultaneously may be useful for cancer therapy. Importantly, the results provide significant insight into the crosstalk between actin and microtubules in regulating the traction force and dynamics of cell deadhesion.
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