Caspase 3, periodically expressed and activated at G2/M transition, is required for nocodazole-induced mitotic checkpoint

S. L. Hsu, C. T.R. Yu, S. C. Yin, M. J. Tang, A. C. Tien, Y. M. Wu, C. Y.F. Huang

Research output: Contribution to journalArticlepeer-review

27 Citations (Scopus)

Abstract

Caspases have been known for several years for their involvement in executing apoptosis, where unwanted or damaged cells are eliminated. Surprisingly, after analysis of the relevant data set from the Stanford microarray database, we noticed that the gene expression pattern for caspase 3, but not for caspase 1, 6, 7, 8, 9, or 10, undergoes periodic change in the HeLa cell cycle. In this study, we have demonstrated that caspase 3, but not other caspases, is upregulated and activated just prior to mitosis. Pretreatment of human hepatoma cells with a caspase 3 inhibitor z-DEVD-FMK, prior to the treatment with an antimicrotubule drug nocodazole, abrogates the mitotic arrest, suggesting that caspase 3 (or a caspase 3-like enzyme) might be involved in mitotic-spindle checkpoint. The studies not only characterize caspase 3 as a cell cycle-regulated protein, but also link the protein to nocodazole-dependent mitotic checkpoint, greatly expanding the understanding of caspase 3.

Original languageEnglish
Pages (from-to)765-771
Number of pages7
JournalApoptosis
Volume11
Issue number5
DOIs
Publication statusPublished - 2006 May 1

All Science Journal Classification (ASJC) codes

  • Pharmacology
  • Pharmaceutical Science
  • Clinical Biochemistry
  • Cell Biology
  • Biochemistry, medical
  • Cancer Research

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