Mechanism of mitotic catastrophe and its role in anticancer therapy

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.

[1]  S. Kaufmann,et al.  Nuclear cGAS suppresses DNA repair and promotes tumorigenesis , 2018, Nature.

[2]  A. Manning,et al.  Aurora A inhibition limits centrosome clustering and promotes mitotic catastrophe in cells with supernumerary centrosomes , 2018, bioRxiv.

[3]  Dan Wang,et al.  Recent advances in microtubule-stabilizing agents. , 2018, European journal of medicinal chemistry.

[4]  B. Tunquist,et al.  A Phase 1 and 2 study of Filanesib alone and in combination with low‐dose dexamethasone in relapsed/refractory multiple myeloma , 2017, Cancer.

[5]  V. Cenklová,et al.  Photodynamic therapy with TMPyP - Porphyrine induces mitotic catastrophe and microtubule disorganization in HeLa and G361 cells, a comprehensive view of the action of the photosensitizer. , 2017, Journal of photochemistry and photobiology. B, Biology.

[6]  Martin A. M. Reijns,et al.  cGAS surveillance of micronuclei links genome instability to innate immunity , 2017, Nature.

[7]  Dennis E Discher,et al.  Mitotic progression following DNA damage enables pattern recognition within micronuclei , 2017, Nature.

[8]  G. Kroemer,et al.  Caspase 2 in mitotic catastrophe: The terminator of aneuploid and tetraploid cells , 2017, Molecular & cellular oncology.

[9]  Nicolai J. Birkbak,et al.  BCL9L Dysfunction Impairs Caspase-2 Expression Permitting Aneuploidy Tolerance in Colorectal Cancer , 2017, Cancer cell.

[10]  M. Czuczman,et al.  Mitotic catastrophe and cell cycle arrest are alternative cell death pathways executed by bortezomib in rituximab resistant B-cell lymphoma cells , 2016, Oncotarget.

[11]  D. Green,et al.  Caspase-2-mediated cell death is required for deleting aneuploid cells , 2016, Oncogene.

[12]  Y. Min,et al.  The Aurora kinase A inhibitor TC-A2317 disrupts mitotic progression and inhibits cancer cell proliferation , 2016, Oncotarget.

[13]  E. Seto,et al.  HDACs and HDAC Inhibitors in Cancer Development and Therapy. , 2016, Cold Spring Harbor perspectives in medicine.

[14]  M. Gee.  Targeting the Mitotic Catastrophe Signaling Pathway in Cancer , 2015 .

[15]  R. Poon,et al.  Co-inhibition of polo-like kinase 1 and Aurora kinases promotes mitotic catastrophe , 2015, Oncotarget.

[16]  F. Camargo,et al.  Cytokinesis Failure Triggers Hippo Tumor Suppressor Pathway Activation , 2014, Cell.

[17]  G. Schwartz,et al.  A Phase I trial of the kinesin spindle protein (Eg5) inhibitor AZD4877 in patients with solid and lymphoid malignancies , 2013, Investigational New Drugs.

[18]  M. Esteller,et al.  Antitumor activity of a small-molecule inhibitor of the histone kinase Haspin , 2011, Oncogene.

[19]  P. C. de Witt Hamer,et al.  WEE1 Kinase Targeting Combined with DNA-Damaging Cancer Therapy Catalyzes Mitotic Catastrophe , 2011, Clinical Cancer Research.

[20]  D. Oh,et al.  Pharmacologic inhibition of the anaphase-promoting complex induces a spindle checkpoint-dependent mitotic arrest in the absence of spindle damage. , 2010, Cancer cell.

[21]  Duane A. Compton,et al.  Proliferation of aneuploid human cells is limited by a p53-dependent mechanism , 2010, The Journal of cell biology.

[22]  L. Galluzzi,et al.  An automated fluorescence videomicroscopy assay for the detection of mitotic catastrophe , 2010, Cell Death and Disease.

[23]  Stephen S. Taylor,et al.  Cancer cells display profound intra- and interline variation following prolonged exposure to antimitotic drugs. , 2008, Cancer cell.

[24]  C. Britten,et al.  G2 checkpoint abrogation and checkpoint kinase-1 targeting in the treatment of cancer , 2008, British Journal of Cancer.

[25]  L. Galluzzi,et al.  Inhibition of Chk1 Kills Tetraploid Tumor Cells through a p53-Dependent Pathway , 2007, PloS one.

[26]  H. Koga,et al.  Cell cycle regulation by the Wee1 Inhibitor PD0166285, Pyrido [2,3-d] pyimidine, in the B16 mouse melanoma cell line , 2006, BMC Cancer.

[27]  Mi Ae Kim,et al.  Two distinct modes of cell death induced by doxorubicin: apoptosis and cell death through mitotic catastrophe accompanied by senescence-like phenotype , 2005, Oncogene.

[28]  H. Saya,et al.  Spindle checkpoint function is required for mitotic catastrophe induced by DNA-damaging agents , 2004, Oncogene.

[29]  G. Kroemer,et al.  Mitotic catastrophe constitutes a special case of apoptosis whose suppression entails aneuploidy , 2004, Oncogene.

[30]  Guido Kroemer,et al.  Cell death by mitotic catastrophe: a molecular definition , 2004, Oncogene.

[31]  J. M. Lee,et al.  p53 regulates a G2 checkpoint through cyclin B1. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[32]  D. Beach,et al.  cdc2 and the regulation of mitosis: six interacting mcs genes. , 1989, Genetics.