Related Experiment Video

Updated: Sep 27, 2025

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis
08:55

Characterization of MLKL-mediated Plasma Membrane Rupture in Necroptosis

Published on: August 7, 2018

11.0K

Necroptosis as a Novel Facet of Mitotic Catastrophe

Aleksandra Yu Egorshina1, Alexey V Zamaraev1, Vitaliy O Kaminskyy2

  • 1Faculty of Medicine, MV Lomonosov Moscow State University, 119991 Moscow, Russia.

International Journal of Molecular Sciences
|April 12, 2022
PubMed

Insights

Mitotic catastrophe, a cell defense against abnormal mitosis, can lead to programmed cell death. This study shows that inhibiting caspases or autophagy can trigger RIP1-dependent necroptosis following mitotic catastrophe.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Mitotic catastrophe eliminates cells with aberrant mitosis via cell-death pathways or senescence.
  • Apoptosis, autophagic cell death, and necrosis are known outcomes of mitotic catastrophe.

Purpose of the Study:

  • To investigate the role of caspase activity and autophagy in the cell death pathways following doxorubicin-induced mitotic catastrophe.
  • To determine if necroptosis can be a consequence of mitotic catastrophe under specific conditions.

Main Methods:

  • Treatment of cells with doxorubicin (600 nM) to induce mitotic catastrophe.
  • Inhibition of caspase activity using chemical inhibitors.
  • Suppression of autophagy via chemical inhibitors or ATG13 knockout.
  • Analysis of cell death pathways, including RIP1-dependent necroptosis.

Main Results:

  • Doxorubicin effectively stimulated mitotic catastrophe.
  • Inhibition of caspase activity resulted in cells with mitotic catastrophe hallmarks and triggered RIP1-dependent necroptosis.
  • Suppression of autophagy upregulated RIP1 phosphorylation and promoted necroptotic cell death.

Conclusions:

  • Mitotic catastrophe can precede necroptosis, in addition to apoptosis and autophagy, under specific experimental conditions.
  • RIP1-dependent necroptosis is a significant cell death pathway activated following mitotic catastrophe when caspases or autophagy are inhibited.
Keywords:
autophagydoxorubicin treatmentmitotic catastrophenecroptosis

More Related Videos

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis12:55

Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis

Published on: February 16, 2015

18.2K
Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells15:53

Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells

Published on: August 21, 2013

15.1K

Related Concept Videos

Necrosis01:16

Necrosis

Necrosis is considered as an “accidental” or unexpected form of cell death that ends in cell lysis. The first noticeable mention of “necrosis” was in 1859 when Rudolf Virchow used this term to describe advanced tissue breakdown in his compilation titled “Cell Pathology”.
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
4.9K
Overview of Cell Death01:30

Overview of Cell Death

Cell death is an essential process where the body gets rid of old or damaged cells. Cell proliferation and death need to be balanced, as an imbalance between the two may lead to cancer or autoimmune diseases.
Cell death was observed in the early 19th century, but there was no experimental evidence to prove it. In 1842, Carl Vogt first discovered cell death in a metamorphic toad; however, it was not termed ‘cell death.’ Scientists discovered different cell death pathways only in the...
7.9K
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and...
3.6K
Microtubule Instability02:17

Microtubule Instability

Microtubules are hollow cylindrical filaments having a diameter of approximately 25 nm and a length that varies from 200 nm to 25 μm. GTP-bound tubulin subunits form αβ-heterodimers for microtubule assembly. These core building blocks interact longitudinally, polymerizing into protofilaments. The protofilaments then interact with one another through lateral bonding forces to form stable cylindrical microtubules. These cylindrical filaments are dynamic as they undergo repeated...
5.3K
Apoptosis01:30

Apoptosis

Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
12.1K
Separation of Sister Chromatids02:17

Separation of Sister Chromatids

At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...
3.8K