ArticleBMC chemical biology2010
Mitotic slippage in non-cancer cells induced by a microtubule disruptor, disorazole C1.
Article in BMC chemical biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- A vertically integrated system for tracking and assessing cell-cycle-aware phenotypes under confinement.APL bioengineering · 2026Article
- Exploration of the Tertiary Amide Chemical Space of Dolastatin 15 Analogs Reveals New Insights into the Structure-Anticancer Activity Relationship.ChemMedChem · 2025Article
- Extending the Structure-Activity Relationship of Disorazole CChembiochem : a European journal of chemical biology · 2022Article
- Stable aneuploid tumors cells are more sensitive to TTK inhibition than chromosomally unstable cell lines.Oncotarget · 2017Article
- Genetic engineering and heterologous expression of the disorazol biosynthetic gene cluster via Red/ET recombineering.Scientific reports · 2016Article
- Bis-cyclopropane analog of disorazole C1 is a microtubule-destabilizing agent active in ABCB1-overexpressing human colon cancer cells.Oncotarget · 2015Article
- Total synthesis of (-)-CP2-disorazole C1.Organic letters · 2011Article
- Molecular and cellular pathways associated with chromosome 1p deletions during colon carcinogenesis.Clinical and experimental gastroenterology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
backgroundDisorazoles are polyene macrodiolides isolated from a myxobacterium fermentation broth. Disorazole C1 was newly synthesized and found to depolymerize microtubules and cause mitotic arrest. Here we examined the cellular responses to disorazole C1 in both non-cancer and cancer cells and compared our results to vinblastine and taxol.
resultsIn non-cancer cells, disorazole C1 induced a prolonged mitotic arrest, followed by mitotic slippage, as confirmed by live cell imaging and cell cycle analysis. This mitotic slippage was associated with cyclin B degradation, but did not require p53. Four assays for apoptosis, including western blotting for poly(ADP-ribose) polymerase cleavage, microscopic analyses for cytochrome C release and annexin V staining, and gel electrophoresis examination for DNA laddering, were conducted and demonstrated little induction of apoptosis in non-cancer cells treated with disorazole C1. On the contrary, we observed an activated apoptotic pathway in cancer cells, suggesting that normal and malignant cells respond differently to disorazole C1.
conclusionOur studies demonstrate that non-cancer cells undergo mitotic slippage in a cyclin B-dependent and p53-independent manner after prolonged mitotic arrest caused by disorazole C1. In contrast, cancer cells induce the apoptotic pathway after disorazole C1 treatment, indicating a possibly significant therapeutic window for this compound.
Identifiers
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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.