title: Benzyl isothiocyanate modifies expression of the G2/M arrest-related genes.
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 G2/M progression that coincided with the apoptosis induction. We demonstrated that BITC significantly up-regulated expression of the G2/M cell cycle arrest-regulating genes including p21, GADD45, and 14-3-3sigma. 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.
authors.affiliation: Laboratory of Food and Biodynamics, Nagoya University Graduate School of Bioagricultural Sciences, Nagoya, Japan.
authors.forename: Noriyuki
authors.initials: N
authors.lastname: Miyoshi
authors.forename: Koji
authors.initials: K
authors.lastname: Uchida
authors.forename: Toshihiko
authors.initials: T
authors.lastname: Osawa
authors.forename: Yoshimasa
authors.initials: Y
authors.lastname: Nakamura
mesh_terms: D016588:Anticarcinogenic Agents / Q000494:pharmacology*; D017209:Apoptosis / Q000187:drug effects; D002453:Cell Cycle / Q000187:drug effects; D002455:Cell Division / Q000187:drug effects / Q000235:genetics*; D016195:G2 Phase / Q000187:drug effects / Q000235:genetics*; D005786:Gene Expression Regulation / Q000187:drug effects*; D018922:HL-60 Cells; D006367:HeLa Cells; D006801:Humans; D017879:Isothiocyanates / Q000494:pharmacology*; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D016588:Anticarcinogenic Agents; D017879:Isothiocyanates; C031403:benzyl isothiocyanate