Related Experiment Video

Updated: Apr 26, 2026

Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
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Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis

Published on: December 5, 2017

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Molecular pathways: regulation and targeting of kinetochore-microtubule attachment in cancer

Jacob A Herman1, Chad M Toledo2, James M Olson3

  • 1Department of Biochemistry and Molecular Biology, Colorado State University, Fort Collins, Colorado.

Clinical Cancer Research : an Official Journal of the American Association for Cancer Research
|August 9, 2014
PubMed

Insights

Oncogene-driven changes in kinetochore regulation, specifically involving BubR1 and BuGZ proteins, may cause chromosome instability in glioblastoma. Targeting these kinetochore-microtubule attachments offers new therapeutic strategies for cancer.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Kinetochores are crucial protein structures that attach centromeric DNA to spindle microtubules during mitosis for chromosome movement.
  • Defects in kinetochore-microtubule (KT-MT) attachments are linked to chromosome instability and cancer progression.
  • The specific causes of KT-MT attachment defects in cancer cells are not well understood.

Purpose of the Study:

  • To investigate oncogene-driven alterations in kinetochore regulation in glioblastoma multiforme (GBM).
  • To identify novel therapeutic targets within kinetochore-associated proteins for GBM and other cancers.

Main Methods:

  • The study focuses on recent findings related to kinetochore regulation in cancer.
  • It specifically examines the roles of BubR1 and BuGZ proteins and their GLE2p-binding domains.
  • Analysis of oncogene-driven changes in kinetochore-microtubule interactions.

Main Results:

  • Evidence suggests oncogene-driven changes in kinetochore regulation occur in GBM.
  • These changes may lead to chromosome instability, a hallmark of cancer.
  • BubR1 and BuGZ proteins are identified as potential therapeutic targets.

Conclusions:

  • Altered kinetochore regulation by oncogenes contributes to chromosome instability in GBM.
  • Targeting kinetochore proteins like BubR1 and BuGZ presents a promising therapeutic avenue for GBM.
  • Further research into KT-MT attachment defects may reveal broader cancer treatment strategies.

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