Related Experiment Video

Updated: Jun 22, 2026

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes
05:22

Generation and Isolation of Cell Cycle-arrested Cells with Complex Karyotypes

Published on: April 13, 2018

The role of aneuploidy in promoting and suppressing tumors

Beth A A Weaver1, Don W Cleveland

  • 1Department of Pharmacology, University of Wisconsin-Madison, Madison, WI 53562, USA. baweaver@wisc.edu

The Journal of Cell Biology
|June 17, 2009
PubMed

Insights

Mitotic checkpoint dysfunction can drive cancer. A study in mice revealed that a mutant Cdc20 protein, bypassing mitotic checkpoint control, caused aneuploidy and high tumor incidence, suggesting dual roles in cancer progression.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • The mitotic checkpoint ensures accurate chromosome segregation during cell division.
  • Cdc20 is a crucial protein targeted by the mitotic checkpoint, regulating anaphase.
  • Dysregulation of mitotic checkpoint signaling is implicated in both tumor suppression and promotion.

Discussion:

  • Li et al. generated mice with a Cdc20 mutant resistant to mitotic checkpoint inhibition.
  • These mice exhibited aneuploidy, a hallmark of genomic instability.
  • A high incidence of tumors was observed in these animals.

Key Insights:

  • The study demonstrates that bypassing mitotic checkpoint control leads to aneuploidy.
  • Persistent aneuploidy, combined with potential non-mitotic roles of mutant Cdc20, contributes to tumor development.
  • This highlights the complex relationship between mitotic fidelity and cancer.

Outlook:

  • Further investigation into the non-mitotic functions of Cdc20 is warranted.
  • Understanding these mechanisms could reveal new therapeutic strategies for cancers with mitotic defects.
  • This research provides a valuable model for studying aneuploidy-driven tumorigenesis.

More Related Videos

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel08:29

Long-term Live-cell Imaging to Assess Cell Fate in Response to Paclitaxel

Published on: May 14, 2018

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia08:14

Induction and Diagnosis of Tumors in Drosophila Imaginal Disc Epithelia

Published on: July 25, 2017

Related Concept Videos

Nondisjunction01:21

Nondisjunction

Nondisjunction is the failure of homologous chromosomes or sister chromatids to separate correctly and move to the opposite poles of the cells. This produces daughter cells with abnormal chromosome numbers.  Nondisjunction is common during anaphase I or anaphase II of meiosis.  Mutations in synaptonemal complex proteins that attach homologous chromosomes increase the chances of nondisjunction in anaphase I of meiosis I. In contrast, mutations in topoisomerases and condensins that hold sister...
Nondisjunction01:29

Nondisjunction

During meiosis, chromosomes occasionally separate improperly. This occurs due to failure of homologous chromosome separation during meiosis I or failed sister chromatid separation during meiosis II. In some species, notably plants, nondisjunction can result in an organism with an entire additional set of chromosomes, which is called polyploidy. In humans, nondisjunction can occur during male or female gametogenesis and the resulting gametes possess one too many or one too few chromosomes.
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...