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Benzyl isothiocyanate modifies expression of the G 2 /M arrest‐related genes
Author(s) -
Miyoshi Noriyuki,
Uchida Koji,
Osawa Toshihiko,
Nakamura Yoshimasa
Publication year - 2004
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.552210106
Subject(s) - benzyl isothiocyanate , phenethyl isothiocyanate , isothiocyanate , apoptosis , cell cycle checkpoint , cell cycle , chemistry , chemoprotective , carcinogenesis , microbiology and biotechnology , mechanism (biology) , gene , cancer research , biology , biochemistry , antioxidant , philosophy , epistemology
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.