Paclitaxel-induced aberrant mitosis and mitotic slippage efficiently lead to proliferative death irrespective of canonical apoptosis and p53

Spindle poisons elicit various cellular responses following metaphase arrest, but how they relate to long-term clonogenicity has remained unclear. We prepared several HeLa lines in which the canonical apoptosis pathway was attenuated, and compared their acute responses to paclitaxel, as well as long...

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Bibliographic Details
Published in:	Cell cycle (Georgetown, Tex.) Vol. 15; no. 23; pp. 3268 - 3277
Main Authors:	Yasuhira, Shinji, Shibazaki, Masahiko, Nishiya, Masao, Maesawa, Chihaya
Format:	Journal Article
Language:	English
Published:	United States Taylor & Francis 01-12-2016
Subjects:	Apoptosis - drug effects Cell Cycle Checkpoints - drug effects Cell Proliferation - drug effects Cell Survival - drug effects Clone Cells Cysteine - analogs & derivatives Cysteine - pharmacology DNA - metabolism Genes, Reporter HeLa Cells Humans Kinesin - antagonists & inhibitors Kinesin - metabolism Melanoma - pathology Mitochondrial Membranes - drug effects Mitochondrial Membranes - metabolism Mitosis - drug effects Paclitaxel - pharmacology Permeability Phenotype Reproducibility of Results Time-Lapse Imaging Tumor Suppressor Protein p53 - metabolism paclitaxel spindle poison mitotic catastrophe mitotic slippage spindle assembly checkpoint apoptosis metaphase arrest Aberrant mitosis
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