The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.
How do anti-mitotic drugs kill cancer cells?
Abstract
In 2007, over 12-million people were diagnosed with cancer. According to the American Cancer Society, at least one third of these individuals are not expected to survive the disease, making cancer the second most prevalent cause of death worldwide. Systemic chemotherapy forms the mainstay of cancer treatment, and agents that disrupt mitotic spindle assembly – so called `anti-mitotics' – are commonly used to treat a wide variety of cancers. Traditional anti-mitotic agents include the microtubule toxins such as taxol, other taxanes and the vinca alkaloids, all of which have proven successful in the clinic. However, patient response remains highly unpredictable, and drug resistance is common. In addition, toxicity is a problem. To address these limitations, a new generation of anti-mitotic drugs is being developed. As the first wave of these new agents enters clinical trails, much hope rests on their outcome. Meanwhile, significant attention is being focused on trying to predict which tumour types are likely to respond. In this Commentary, we outline recent advances in our understanding of how cancer cells respond to anti-mitotic drugs, and discuss the relevance of these studies to their use in the clinic.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“When they exit mitosis, several post-mitotic responses occur that can lead to cell death, including cell-cycle arrest and apoptosis [14].”
From Targeted Nano-Drug Delivery of Colchicine against Colon Cancer Cells by Means of Mesoporous Silica Nanoparticles (2020) · cites this paper as [14]
In the citing paper
“Because COL inhibits tubulin, the post-antimitotic response resulted in various molecular pathways, including cell-cycle arrest, apoptosis, and genetic regulation [14].”
From Targeted Nano-Drug Delivery of Colchicine against Colon Cancer Cells by Means of Mesoporous Silica Nanoparticles (2020) · cites this paper as [14]
Citations
Cites
The spindle-assembly checkpoint in space and time
Musacchio, A., & Salmon, E. D. (2007) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2163 · Cited by 2,227
Research works printed but not linked: 34
- Allan, L. A. and Clarke, P. R. (2007). Phosphorylation of caspase-9 by CDK1/cyclin B1 protects mitotic cells against apoptosis. Mol. Cell26, 301-310. · DOI
- Bergnes, G., Brejc, K. and Belmont, L. (2005). Mitotic kinesins: prospects for antimitotic drug discovery. Curr. Top. Med. Chem.5, 127-145. · DOI
- Brinkley, B. R. (2001). Managing the centrosome numbers game: from chaos to stability in cancer cell division. Trends Cell Biol.11, 18-21. · DOI
- Brito, D. A. and Rieder, C. L. (2006). Mitotic checkpoint slippage in humans occurs via cyclin B destruction in the presence of an active checkpoint. Curr. Biol.16, 1194-1200. · DOI
- Brito, D. A. and Rieder, C. L. (2008). The ability to survive mitosis in the presence of microtubule poisons differs significantly between human nontransformed (RPE-1) and cancer (U2OS, HeLa) cells. Cell Motil. Cytoskeleton (in press). doi:10.1002/cm.20316. · DOI
- Brito, D. A., Yang, Z. and Rieder, C. L. (2008). Microtubules do not promote mitotic slippage when the spindle assembly checkpoint cannot be satisfied. J. Cell Biol.182, 623-629. · DOI
- Gascoigne, K. E. and Taylor, S. S. (2008). Cancer cells display profound intra- and interline variation following prolonged exposure to antimitotic drugs. Cancer Cell14, 111-122. · DOI · Paper page
- Holland, A. J. and Cleveland, D. W. (2008). Beyond genetics: surprising determinants of cell fate in antitumor drugs. Cancer Cell14, 103-105. · DOI
- Jordan, M. A. and Wilson, L. (2004). Microtubules as a target for anticancer drugs. Nat. Rev. Cancer4, 253-265. · DOI · Paper page
- Jordan, M. A., Toso, R. J., Thrower, D. and Wilson, L. (1993). Mechanism of mitotic block and inhibition of cell proliferation by taxol at low concentrations. Proc. Natl. Acad. Sci. USA90, 9552-9556. · DOI · Paper page
- Karlsson, M. O., Molnar, V., Freijs, A., Nygren, P., Bergh, J. and Larsson, R. (1999). Pharmacokinetic models for the saturable distribution of paclitaxel. Drug Metab. Dispos.27, 1220-1223. · DOI
- Keen, N. and Taylor, S. (2004). Aurora-kinase inhibitors as anticancer agents. Nat. Rev. Cancer4, 927-936. · DOI
- Keen, N. and Taylor, S. (2009). Mitotic drivers-inhibitors of the Aurora B Kinase. Cancer Metastasis Rev.28, 185-195. · DOI
- Klein, E., Debonis, S., Thiede, B., Skoufias, D. A., Kozielski, F. and Lebeau, L. (2007). New chemical tools for investigating human mitotic kinesin Eg5. Bioorg. Med. Chem.15, 6474-6488. · DOI
- Knox, J. J., Gill, S., Synold, T. W., Biagi, J. J., Major, P., Feld, R., Cripps, C., Wainman, N., Eisenhauer, E. and Seymour, L. (2008). A phase II and pharmacokinetic study of SB-715992, in patients with metastatic hepatocellular carcinoma: a study of the National Cancer Institute of Canada Clinical Trials Group (NCIC CTG IND.168). Invest. New Drugs26, 265-272. · DOI
- Kwon, M., Godinho, S. A., Chandhok, N. S., Ganem, N. J., Azioune, A., Thery, M. and Pellman, D. (2008). Mechanisms to suppress multipolar divisions in cancer cells with extra centrosomes. Genes Dev.22, 2189-2203. · DOI
- Lanni, J. S. and Jacks, T. (1998). Characterization of the p53-dependent postmitotic checkpoint following spindle disruption. Mol. Cell. Biol.18, 1055-1064. · DOI
- Lee, C. W., Belanger, K., Rao, S. C., Petrella, T. M., Tozer, R. G., Wood, L., Savage, K. J., Eisenhauer, E. A., Synold, T. W., Wainman, N. et al. (2008). A phase II study of ispinesib (SB-715992) in patients with metastatic or recurrent malignant melanoma: a National Cancer Institute of Canada Clinical Trials Group trial. Invest. New Drugs26, 249-255. · DOI
- McGrogan, B. T., Gilmartin, B., Carney, D. N. and McCann, A. (2008). Taxanes, microtubules and chemoresistant breast cancer. Biochim. Biophys. Acta1785, 96-132. · DOI
- Milross, C. G., Mason, K. A., Hunter, N. R., Chung, W. K., Peters, L. J. and Milas, L. (1996). Relationship of mitotic arrest and apoptosis to antitumor effect of paclitaxel. J. Natl. Cancer Inst.88, 1308-1314. · DOI
- Niikura, Y., Dixit, A., Scott, R., Perkins, G. and Kitagawa, K. (2007). BUB1 mediation of caspase-independent mitotic death determines cell fate. J. Cell Biol.178, 283-296. · DOI
- Nogales, E. (2000). Structural insights into microtubule function. Annu. Rev. Biochem.69, 277-302. · DOI
- Orth, J. D., Tang, Y., Shi, J., Loy, C. T., Amendt, C., Wilm, C., Zenke, F. T. and Mitchison, T. J. (2008). Quantitative live imaging of cancer and normal cells treated with Kinesin-5 inhibitors indicates significant differences in phenotypic responses and cell fate. Mol. Cancer Ther.7, 3480-3489. · DOI
- Rai, S. S. and Wolff, J. (1996). Localization of the vinblastine-binding site on beta-tubulin. J. Biol. Chem.271, 14707-14711. · DOI
- Rieder, C. L. and Maiato, H. (2004). Stuck in division or passing through: what happens when cells cannot satisfy the spindle assembly checkpoint. Dev. Cell7, 637-651. · DOI
- Rowinsky, E. K. (1997). The development and clinical utility of the taxane class of antimicrotubule chemotherapy agents. Annu. Rev. Med.48, 353-374. · DOI
- Schiff, P. B., Fant, J. and Horwitz, S. B. (1979). Promotion of microtubule assembly in vitro by taxol. Nature277, 665-667. · DOI · Paper page
- Schimming, R., Mason, K. A., Hunter, N., Weil, M., Kishi, K. and Milas, L. (1999). Lack of correlation between mitotic arrest or apoptosis and antitumor effect of docetaxel. Cancer Chemother. Pharmacol.43, 165-172. · DOI
- Schwartz, E. L. (2009). Antivascular actions of microtubule-binding drugs. Clin. Cancer Res.15, 2594-2601. · DOI
- Shi, J., Orth, J. D. and Mitchison, T. (2008). Cell type variation in responses to antimitotic drugs that target microtubules and kinesin-5. Cancer Res.68, 3269-3276. · DOI
- Strebhardt, K. and Ullrich, A. (2006). Targeting polo-like kinase 1 for cancer therapy. Nat. Rev. Cancer6, 321-330. · DOI
- Tang, P. A., Siu, L. L., Chen, E. X., Hotte, S. J., Chia, S., Schwarz, J. K., Pond, G. R., Johnson, C., Colevas, A. D., Synold, T. W. et al. (2008). Phase II study of ispinesib in recurrent or metastatic squamous cell carcinoma of the head and neck. Invest. New Drugs26, 257-264. · DOI
- Tao, W., South, V. J., Zhang, Y., Davide, J. P., Farrell, L., Kohl, N. E., Sepp-Lorenzino, L. and Lobell, R. B. (2005). Induction of apoptosis by an inhibitor of the mitotic kinesin KSP requires both activation of the spindle assembly checkpoint and mitotic slippage. Cancer Cell8, 49-59. · DOI
- Weaver, B. A. and Cleveland, D. W. (2005). Decoding the links between mitosis, cancer, and chemotherapy: the mitotic checkpoint, adaptation, and cell death. Cancer Cell8, 7-12. · DOI
Cited by
Sorted by citations
Antibody–Drug Conjugates: An Emerging Concept in Cancer Therapy
Chari, R. V. J., Miller, M. L., & Widdison, W. C. (2014) · Angewandte Chemie International Edition · doi:10.1002/anie.201307628 · Cited by 930
Giladi, M., Schneiderman, R. S., Voloshin, T., Porat, Y., Munster, M., Blat, R., Sherbo, S., Bomzon, Z., Urman, N., Itzhaki, A., et al. (2015) · Scientific Reports · doi:10.1038/srep18046 · Cited by 327
USP7 Is a Master Regulator of Genome Stability
Valles, G. J., Bezsonova, I., Woodgate, R., & Ashton, N. W. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.00717 · Cited by 114
“Taxanes, in this way, prevent proper chromosome orientation on the metaphase plate, leading to activation of the spindle-assembly checkpoint and stalling cells at the metaphase to anaphase transition (Musacchio and Salmon, 2007; Gascoigne and Taylor, 2009).”
BackgroundMitotic catastrophe and cancer drug resistance: A link that must to be broken
Denisenko, T. V., Sorokina, I. V., Gogvadze, V., & Zhivotovsky, B. (2016) · Drug Resistance Updates · doi:10.1016/j.drup.2015.11.002 · Cited by 108
AbouAitah, K., Hassan, H. A., Swiderska-Sroda, A., Gohar, L., Shaker, O. G., Wojnarowicz, J., Opalinska, A., Smalc-Koziorowska, J., Gierlotka, S., & Lojkowski, W. (2020) · Cancers · doi:10.3390/cancers12010144 · Cited by 105
Metadata
- Authors
- Gascoigne, K. E., & Taylor, S. S.
- Affiliations
- Faculty of Life Sciences, University of Manchester, Michael Smith Building, Oxford Road, Manchester, M13 9PT, UK
- Venue
- Journal of Cell Science
- Publisher
- The Company of Biologists
- Published
- 2009-08-01
- Volume
- 122
- Issue
- 15
- Pages
- 2579-2585
- ISSN
- 1477-9137
- 0021-9533
- Cited by
- 327
- References
- 1
- Language
- en
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
How to cite
Cite CoChat for the checks on this page, and the paper for its own findings.
- This page
- CoChat. (2026). Citation check: How do anti-mitotic drugs kill cancer cells? https://app.cochat.ai/papers/10.1242/jcs.039719
- The paper
- Gascoigne, K. E., & Taylor, S. S. (2009). How do anti-mitotic drugs kill cancer cells? Journal of Cell Science. https://doi.org/10.1242/jcs.039719