Rapid proliferation of daughter cells lacking particular chromosomes due to multipolar mitosis promotes clonal evolution in colorectal cancer cells

Chao Yang, Xiaoyun Shi, Yun Huang, Zhen Zhang, Howard J Cooke, Mingrong Wang, Qinghua Shi

Research output: Contribution to journalArticlepeer-review

Abstract

Aneuploidy and chromosome instability (CIN) are hallmarks of the vast majority of solid tumors. However, the origins of aneuploid cells are unknown. The aim of this study is to improve our understanding of how aneuploidy and/or CIN arise and of karyotype evolution in cancer cells. By using fluorescence in situ hybridization (FISH) on cells after long-term live cell imaging, we demonstrated that most (> 90%) of the newly generated aneuploid cells resulted from multipolar divisions. Multipolar division occurred in mononucleated and binucleated parental cells, resulting in variation of chromosome compositions in daughter cells. These karyotypes can have the same chromosome number as their mother clone or lack a copy of certain chromosomes. Interestingly, daughter cells that lost a chromosome were observed to survive and form clones with shorter cell cycle duration. In our model of cancer cell evolution, the rapid proliferation of daughter cells from multipolar mitosis promotes colonal evolution in colorectal cancer cells.
Original languageEnglish
Pages (from-to)2650-9
Number of pages10
JournalCell Cycle
Volume11
Issue number14
DOIs
Publication statusPublished - 15 Jul 2012

Keywords

  • Aneuploidy
  • Cell Line, Tumor
  • Cell Proliferation
  • Chromosomal Instability
  • Chromosomes
  • Clonal Evolution
  • Colorectal Neoplasms
  • HCT116 Cells
  • HT29 Cells
  • Humans
  • Karyotyping
  • Mitosis

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