ArticleMolecular cancer therapeutics2011
Overexpression of mitotic centromere-associated Kinesin stimulates microtubule detachment and confers resistance to paclitaxel.
Article in Molecular cancer therapeutics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 86 citations in OpenAlex.
- Kinesins in Cancer Drug Resistance: Mechanisms, Therapeutic Targeting, and Translational Potential.Cancers · 2026Review
- The Clinical Significance of KIFs in Cervical and Endometrial Cancer: from Mechanisms to Biomarker and Therapeutic Potential.Reproductive sciences (Thousand Oaks, Calif.) · 2026Review
- From Motor Proteins to Oncogenic Factors: The Evolving Role of Kinesin Superfamily Proteins in Breast Cancer Development.Molecular biotechnology · 2026Review
- Low KIF26B Expression Reduces Paclitaxel Resistance and Predicts Good Prognosis in Ovarian Cancer.Current issues in molecular biology · 2026Article
- FOXM1 Signaling Network Transcriptionally Upregulates Expression of Proteins Involved in Mitotic Progression to Induce High Proliferation and Chromosomal Instability in Androgen Receptor-Low Triple-Negative Breast Cancer.International journal of molecular sciences · 2026Article
- Review
- The role of kinesin family members in hepatobiliary carcinomas: from bench to bedside.Biomarker research · 2024Review
- EGFR-mediated hyperacetylation of tubulin induced docetaxel resistance by downregulation of HDAC6 and upregulation of MCAK and PLK1 in prostate cancer cells.The Kaohsiung journal of medical sciences · 2024Article
- Bioinformatical analysis of the key differentially expressed genes for screening potential biomarkers in Wilms tumor.Scientific reports · 2023Article
- Article
- α-Tubulin detyrosination links the suppression of MCAK activity with taxol cytotoxicity.The Journal of cell biology · 2023Article
- Cell cycle dysregulation with overexpression of KIF2C/MCAK is a critical event in nasopharyngeal carcinoma.Genes & diseases · 2023Article
- Combination of Paclitaxel and PXR Antagonist SPA70 Reverses Paclitaxel-Resistant Non-Small Cell Lung Cancer.Cells · 2022Article
- Personalized medicine of non-gene-specific chemotherapies for non-small cell lung cancer.Acta pharmaceutica Sinica. B · 2021Review
- TBX15/miR-152/KIF2C pathway regulates breast cancer doxorubicin resistance via promoting PKM2 ubiquitination.Cancer cell international · 2021Article
- Spatial regulation of MCAK promotes cell polarization and focal adhesion turnover to drive robust cell migration.Molecular biology of the cell · 2021Article
- α-Tubulin detyrosination impairs mitotic error correction by suppressing MCAK centromeric activity.The Journal of cell biology · 2020Article
- Overexpression of kinesin superfamily members as prognostic biomarkers of breast cancer.Cancer cell international · 2020Article
- Inhibition of kinesin family member 20B sensitizes hepatocellular carcinoma cell to microtubule-targeting agents by blocking cytokinesis.Cancer science · 2018Article
- Review
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Numerous studies have implicated mutations in tubulin or the overexpression of specific tubulin genes in resistance to microtubule-targeted drugs. Much less is known about the role of accessory proteins that modulate microtubule behavior in the genesis of drug resistance. Here, we examine mitotic centromere-associated kinesin (MCAK), a member of the kinesin family of microtubule motor proteins that has the ability to stimulate microtubule depolymerization, and show that overexpressing the protein confers resistance to paclitaxel and epothilone A, but increases sensitivity to colcemid. Cells transfected with FLAG-tagged MCAK cDNA using a tet-off-regulated expression system had a disrupted microtubule cytoskeleton and were able to survive a toxic concentration of paclitaxel in the absence, but not in the presence of tetracycline, showing that drug resistance was caused by ectopic MCAK production. Moreover, a population that was heterogeneous with respect to FLAG-MCAK expression became enriched with cells that produced the ectopic protein when it was placed under paclitaxel selection. Similar to previously isolated mutants with altered tubulin, paclitaxel resistant cells resulting from MCAK overexpression were found to have decreased microtubule polymer and a seven-fold increase in the frequency of microtubule detachment from centrosomes. These data are consistent with a model for paclitaxel resistance that is based on stability of the attachment of microtubules to their nucleating centers, and they implicate MCAK in the mechanism of microtubule detachment.
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Registered trials
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