Related Experiment Video

Updated: Oct 2, 2026

Evaluation of the Spindle Assembly Checkpoint Integrity in Mouse Oocytes
10:09

Evaluation of the Spindle Assembly Checkpoint Integrity in Mouse Oocytes

Published on: September 13, 2022

Significance of MAD2 expression to mitotic checkpoint control in ovarian cancer cells

Xianghong Wang1, Dong-Yan Jin, Raymond W M Ng

  • 1Department of Anatomy, Faculty of Medicine, University of Hong Kong, Hong Kong.

Cancer Research
|March 26, 2002
PubMed

Insights

Ovarian cancer cells often show chromosome instability. Reduced MAD2 protein levels impair the mitotic checkpoint, leading to errors in chromosome segregation. Restoring MAD2 can fix this checkpoint defect.

Area of Science:

  • Oncology
  • Cell Biology
  • Genetics

Background:

  • Chromosome instability is a hallmark of ovarian carcinoma.
  • The mitotic checkpoint ensures accurate chromosome segregation, with MAD2 being a crucial protein.
  • Understanding MAD2's role is vital for targeting chromosome instability in cancer.

Purpose of the Study:

  • To investigate mitotic checkpoint function in ovarian cancer cell lines.
  • To determine the relationship between MAD2 protein expression and checkpoint competence.
  • To explore the therapeutic potential of restoring MAD2 levels.

Main Methods:

  • Assessed mitotic checkpoint function in seven ovarian cancer cell lines upon microtubule disruption.
  • Quantified MAD2 protein expression in these cell lines.
  • Utilized an inducible expression system to modulate MAD2 levels in checkpoint-defective cells.

Main Results:

  • 43% of tested ovarian cancer cell lines exhibited defective mitotic checkpoint control.
  • Loss of checkpoint function correlated with reduced MAD2 protein expression.
  • Inducible expression of MAD2 restored mitotic checkpoint function in defective cell lines.

Conclusions:

  • Cellular MAD2 levels act as a molecular switch for mitotic checkpoint control.
  • Defective MAD2 expression contributes to chromosome instability in ovarian cancer.
  • Targeting MAD2 may offer a strategy for novel ovarian cancer therapies.

More Related Videos

Studying Mitotic Checkpoint by Illustrating Dynamic Kinetochore Protein Behavior and Chromosome Motion in Living Drosophila Syncytial Embryos13:59

Studying Mitotic Checkpoint by Illustrating Dynamic Kinetochore Protein Behavior and Chromosome Motion in Living Drosophila Syncytial Embryos

Published on: June 14, 2012

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer09:08

Integration of Bioinformatics Approaches and Experimental Validations to Understand the Role of Notch Signaling in Ovarian Cancer

Published on: January 12, 2020

Related Concept Videos

Meiosis II02:02

Meiosis II

Meiosis II entails cell division and segregation of the sister chromatids, resulting in the production of four unique haploid gametes. The steps for meiosis II are similar to mitosis, except that meiosis II occurs in haploid cells, whereas mitosis occurs in diploid cells.
The timing and cell division patterns of meiosis differ between males and females. In male meiosis, the centrosomes are part of the formation of the meiotic spindle. However, in oocytes, including that of humans, Drosophila,...
The Spindle Assembly Checkpoint02:19

The Spindle Assembly Checkpoint

The spindle assembly checkpoint is a molecular surveillance mechanism ensuring the fidelity of chromosome segregation during anaphase. The checkpoint monitors the completion of all the prerequisite steps before chromosome segregation to determine whether the segregation process should proceed or be delayed.
Many proteins function together to control the spindle assembly checkpoint. Mutations affecting these proteins may allow cells to proceed into anaphase prematurely, resulting in the...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...