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Combining Mitotic Cell Synchronization and High Resolution Confocal Microscopy to Study the Role of Multifunctional Cell Cycle Proteins During Mitosis
08:33

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

Mitotic centromere-associated kinase (MCAK/Kif2C) regulates cellular senescence in human primary cells through a

Mi-Ri Gwon1, Jung Hee Cho, Jae-Ryong Kim

  • 1Department of Biochemistry and Molecular Biology, Aging-associated Vascular Disease Research Center, College of Medicine, Yeungnam University, Daegu 705-717, Republic of Korea.

FEBS Letters
|October 27, 2012
PubMed

Insights

Mitotic centromere-associated kinase (MCAK/Kif2C) is crucial for cell division and its expression decreases during cellular senescence. Reduced MCAK/Kif2C induces senescence, while its restoration can reverse aging phenotypes.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Aging Research

Background:

  • Mitotic centromere-associated kinase (MCAK/Kif2C) is essential for chromosome segregation via microtubule depolymerization.
  • The precise role of MCAK/Kif2C in cellular senescence is not well understood.

Purpose of the Study:

  • To investigate the role of MCAK/Kif2C in the regulation of cellular senescence.
  • To determine the molecular pathways involved in MCAK/Kif2C-mediated senescence.

Main Methods:

  • Analysis of MCAK/Kif2C expression in human primary cells undergoing replicative and premature senescence.
  • Manipulation of MCAK/Kif2C levels (down-regulation and overexpression) in young and old cells.
  • Assessment of senescence phenotypes, including the involvement of p16 and p53 pathways.

Main Results:

  • MCAK/Kif2C expression was found to be reduced in senescent human primary cells.
  • Down-regulation of MCAK/Kif2C in young cells induced premature senescence.
  • Overexpression of MCAK/Kif2C in aged cells partially reversed senescence phenotypes.
  • Senescence induction by MCAK/Kif2C knockdown was dependent on p16 but independent of p53.

Conclusions:

  • MCAK/Kif2C plays a significant role in regulating cellular senescence.
  • The p53-dependent pathway is involved in MCAK/Kif2C-mediated senescence.
  • Modulating MCAK/Kif2C levels may impact organismal aging and cancer prevention.

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