RRC ID 42288
Author Miyoshi N, Uchida K, Osawa T, Nakamura Y.
Title Benzyl isothiocyanate modifies expression of the G2/M arrest-related genes.
Journal Biofactors
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.
Volume 21(1-4)
Pages 23-6
Published 2004-1-1
DOI 10.1002/biof.552210106
PMID 15630165
MeSH Anticarcinogenic Agents / pharmacology* Apoptosis / drug effects Cell Cycle / drug effects Cell Division / drug effects Cell Division / genetics* G2 Phase / drug effects G2 Phase / genetics* Gene Expression Regulation / drug effects* HL-60 Cells HeLa Cells Humans Isothiocyanates / pharmacology* Reverse Transcriptase Polymerase Chain Reaction
IF 4.734
Times Cited 23
WOS Category ENDOCRINOLOGY & METABOLISM BIOCHEMISTRY & MOLECULAR BIOLOGY
Resource
Human and Animal Cells