Benzyl isothiocyanate modifies expression of the G2/M arrest-related genes

Noriyuki Miyoshi, Koji Uchida, Toshihiko Osawa, Yoshimasa Nakamura

Research output: Contribution to journalArticlepeer-review

25 Citations (Scopus)


Naturally occurring isothiocyanates are effective chemoprotective agents against chemical carcinogenesis in experimental animals. In the present study, we clarified the molecular mechanism underlying the relationship between benzyl isothiocyanate (BITC)-induced cell cycle arrest and apoptosis. The exposure of HL-60 cells to BITC resulted in the inhibition of the G_{2}/M progression that coincided with the apoptosis induction. We demonstrated that BITC significantly up-regulated expression of the G_{2}/M cell cycle arrest-regulating genes including p21, GADD45, and 14-3-3σ. Thus, these gathered data further supported that BITC has a potential to induce apoptosis selectively in the proliferating pre-cancerous cells through a cell cycle arrest-dependent mechanism.

Original languageEnglish
Pages (from-to)23-26
Number of pages4
Issue number1-4
Publication statusPublished - Jan 1 2004
Externally publishedYes


  • Apoptosis
  • Benzyl isothiocyanate
  • Cell cycle arrest
  • GADD45
  • p21

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Medicine
  • Clinical Biochemistry


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