Affiliations: Laboratory of Food and Biodynamics, Nagoya University
Graduate School of Bioagricultural Sciences, Nagoya, Japan
Note: [] Address for correspondence: Yoshimasa Nakamura, Laboratory of
Food and Biodynamics, Nagoya University Graduate School of Bioagricultural
Sciences, Nagoya 464-8601, Japan. Tel.: +81 52 789 4126; Fax: +81 52 789 5296;
E-mail: [email protected]
Abstract: 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.
