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Mechanisms to suppress multipolar divisions in cancer cells with extra centrosomes

Mijung Kwon1, Susana A Godinho, Namrata S Chandhok

  • 1Department of Pediatric Oncology, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA 02115, USA.

Genes & Development
|July 30, 2008
PubMed

Insights

Cancer cells with extra centrosomes divide successfully due to mechanisms suppressing multipolar mitoses. Cell shape and adhesion influence mitosis, revealing HSET as a potential therapeutic target for specific cancers.

Area of Science:

  • Cell Biology
  • Cancer Biology
  • Genetics

Background:

  • Multiple centrosomes in tumor cells can cause multipolar divisions, leading to aneuploidy and cell death.
  • However, cancer cells possess mechanisms to suppress multipolar mitoses and ensure successful cell division.

Purpose of the Study:

  • To identify mechanisms that suppress multipolar mitoses in cancer cells.
  • To explore the role of cell shape and adhesion in mitosis of cells with extra centrosomes.
  • To identify potential cancer-selective therapeutic targets.

Main Methods:

  • Genome-wide RNAi screen in Drosophila S2 cells.
  • Secondary analysis in human cancer cells.
  • Live cell imaging and fibronectin micropatterns.

Main Results:

  • Identified novel roles for the spindle assembly checkpoint, cortical actin cytoskeleton, and cell adhesion in suppressing multipolar mitoses.
  • Demonstrated that interphase cell shape and adhesion pattern influence the success of mitosis in cells with extra centrosomes.
  • Found HSET, a kinesin motor, to be essential for the viability of certain extra centrosome-containing cancer cells.

Conclusions:

  • Mechanisms suppressing multipolar mitoses are crucial for cancer cell survival.
  • Cellular morphology and adhesion patterns are linked to mitotic success in aneuploid cancer cells.
  • HSET represents a potential cancer-selective therapeutic target, highlighting the link between cancer cell morphology and unique genetic vulnerabilities.

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