Benzyl isothiocyanate modifies expression of the G 2 /M arrest‐related genes
2004; Wiley; Volume: 21; Issue: 1-4 Linguagem: Inglês
10.1002/biof.552210106
ISSN1872-8081
AutoresNoriyuki Miyoshi, Kôji Uchida, Toshihiko Osawa, Yoshimasa Nakamura,
Tópico(s)Synthesis and Biological Evaluation
ResumoAbstract 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.
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