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Mechanism of mitotic catastrophe and its role in anticancer therapy

Authors :
Dariusz Grzanka
Karolina Warda
Anna Klimaszewska-Wiśniewska
Alina Grzanka
Source :
Postępy Higieny i Medycyny Doświadczalnej, Vol 74, Pp 84-93 (2020)
Publication Year :
2020
Publisher :
Walter de Gruyter GmbH, 2020.

Abstract

The definition of mitotic catastrophe has been the subject of scientific discussion for over a decade. Initially, it was thought that mitotic catastrophe is one of the types of cell death occurring during aberrant mitosis. A number of studies carried out in recent years allowed for a better understanding of the function of this process. According to the definition proposed by the Nomenclature Committee on Cell Death in 2018, mitotic catastrophe is an oncosuppressive mechanism that inhibits the proliferation and/or survival of cells that are unable to complete mitosis by inducing cell death or initiating cellular senescence. Mitotic catastrophe is recognized based on unique nuclear changes, the presence of abnormal mitotic figures and several molecular alterations. It is believed that avoiding mitotic catastrophe by genetically unstable cells promotes their unlimited growth, which can lead to cancer transformation. Therefore, the induction of mitotic catastrophe seems to be a promising strategy for the prevention and treatment of cancer. However, despite the significant role of this process, the molecular events between aberrant mitosis and cell death are still not well understood. It can be assumed that a thorough understanding of signaling pathways linking mitotic catastrophe with cell death will enable the effective use of known inducers of mitotic catastrophe in the treatment of cancer and provide new therapeutic targets. The aim of this review is to present a morphological and functional definition of mitotic catastrophe and its potential role in anticancer therapy.

Details

ISSN :
17322693 and 00325449
Volume :
74
Database :
OpenAIRE
Journal :
Postępy Higieny i Medycyny Doświadczalnej
Accession number :
edsair.doi.dedup.....40b4848656e815a2c2cf1e0dd66c3ed7
Full Text :
https://doi.org/10.5604/01.3001.0014.1328