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Distinct effects of heat shock temperatures on mitotic progression by influencing the spindle assembly checkpoint
Bibliographic Information
- Published
- 2023-08
- Resource Type
- journal article
- Rights Information
-
- https://www.elsevier.com/tdm/userlicense/1.0/
- https://www.elsevier.com/legal/tdmrep-license
- https://doi.org/10.15223/policy-017
- https://doi.org/10.15223/policy-037
- https://doi.org/10.15223/policy-012
- https://doi.org/10.15223/policy-029
- https://doi.org/10.15223/policy-004
- DOI
-
- 10.1016/j.yexcr.2023.113672
- Publisher
- Elsevier BV
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Description
Heat shock is a physiological and environmental stress that leads to the denaturation and inactivation of cellular proteins and is used in hyperthermia cancer therapy. Previously, we revealed that mild heat shock (42 °C) delays the mitotic progression by activating the spindle assembly checkpoint (SAC). However, it is unclear whether SAC activation is maintained at higher temperatures than 42 °C. Here, we demonstrated that a high temperature of 44 °C just before mitotic entry led to a prolonged mitotic delay in the early phase, which was shortened by the SAC inhibitor, AZ3146, indicating SAC activation. Interestingly, mitotic slippage was observed at 44 °C after a prolonged delay but not at 42 °C heat shock. Furthermore, the multinuclear cells were generated by mitotic slippage in 44 °C-treated cells. Immunofluorescence analysis revealed that heat shock at 44 °C reduces the kinetochore localization of MAD2, which is essential for mitotic checkpoint activation, in nocodazole-arrested mitotic cells. These results indicate that 44 °C heat shock causes SAC inactivation even after full activation of SAC and suggest that decreased localization of MAD2 at the kinetochore is involved in heat shock-induced mitotic slippage, resulting in multinucleation. Since mitotic slippage causes drug resistance and chromosomal instability, we propose that there may be a risk of cancer malignancy when the cells are exposed to high temperatures.
Journal
-
- Experimental Cell Research
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Experimental Cell Research 429 (2), 113672-, 2023-08
Elsevier BV