ArticlePloS one2016
Cell Division Cycle 6 Promotes Mitotic Slippage and Contributes to Drug Resistance in Paclitaxel-Treated Cancer Cells.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Comprehensive analysis of multi Ewing sarcoma microarray datasets identifies several prognosis biomarkers.Molecular medicine reports · 2018Pooled it
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- Interaction between CDC6 and Tmod3 accelerates resistance to paclitaxel through focal adhesion assembly.Signal transduction and targeted therapy · 2025Article
- SETDB1 is critically required for uveal melanoma growth and represents a promising therapeutic target.Cell death & disease · 2025Article
- DNA Replication Licensing Factors: Novel Targets for Cancer Therapy via Inhibiting the Stemness of Cancer Cells.International journal of biological sciences · 2022Review
- High Matrix Metalloproteinase 28 Expression is Associated with Poor Prognosis in Pancreatic Adenocarcinoma.OncoTargets and therapy · 2021Article
- Cdc6 disruption leads to centrosome abnormalities and chromosome instability in pancreatic cancer cells.Scientific reports · 2020Article
- Cancer Cell enters reversible quiescence through Intracellular Acidification to resist Paclitaxel Cytotoxicity.International journal of medical sciences · 2020Article
- Insight into norcantharidin, a small-molecule synthetic compound with potential multi-target anticancer activities.Chinese medicine · 2020Review
- The balance between mitotic death and mitotic slippage in acute leukemia: a new therapeutic window?Journal of hematology & oncology · 2019Review
- Resistance to anti-microtubule drug-induced cell death is determined by regulation of BimEL expression.Oncogene · 2019Article
- Imbalance of the spindle-assembly checkpoint promotes spindle poison-mediated cytotoxicity with distinct kinetics.Cell death & disease · 2019Article
- Dysregulation in Actin Cytoskeletal Organization Drives Increased Stiffness and Migratory Persistence in Polyploidal Giant Cancer Cells.Scientific reports · 2018Article
- Construction and Identification of Recombinant HEK293T Cell Lines Expressing Non-structural Protein 1 of Zika Virus.International journal of medical sciences · 2017Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Paclitaxel (PTX) is an antimitotic drug that possesses potent anticancer activity, but its therapeutic potential in the clinic has been hindered by drug resistance. Here, we report a mechanism by which cancer cells can exit from the PTX-induced mitotic arrest, i.e. mitotic slippage, and avoid subsequent death resulting in drug resistance. In cells experiencing mitotic slippage, Cdc6 protein level was significantly upregulated, Cdk1 activity was inhibited, and Cohesin/Rad21 was cleaved as a result. Cdc6 depletion by RNAi or Norcantharidin inhibited PTX-induced Cdc6 up-regulation, maintained Cdk1 activity, and repressed Cohesin/Rad21 cleavage. In all, this resulted in reduced mitotic slippage and reversal of PTX resistance. Moreover, in synchronized cells, the role of Cdc6 in mitotic exit under PTX pressure was also confirmed. This study indicates that Cdc6 may promote mitotic slippage by inactivation of Cdk1. Targeting of Cdc6 may serve as a promising strategy for enhancing the anticancer activity of PTX.
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