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Cell death in the colorectal cancer cell line HT29 in response to glucosinolate metabolites
Author(s) -
Lund Elizabeth K,
Smith Tracy K,
Clarke Rosemary G,
Johnson Ian T
Publication year - 2001
Publication title -
journal of the science of food and agriculture
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 142
eISSN - 1097-0010
pISSN - 0022-5142
DOI - 10.1002/jsfa.904
Subject(s) - cruciferous vegetables , apoptosis , glucosinolate , chemistry , phenethyl isothiocyanate , sulforaphane , annexin , cell culture , isothiocyanate , cell growth , programmed cell death , biochemistry , cancer cell , benzyl isothiocyanate , cancer research , cancer , biology , botany , genetics , brassica
Glucosinolate breakdown products are potential anti‐carcinogenic phytochemicals derived from cruciferous vegetables. This study compared the induction of apoptosis in colorectal adenocarcinoma cells (HT29) by four isothiocyanates (ITC) benzyl‐ITC, allyl‐ITC (AITC), phenylethyl‐ITC (PEITC) and methylsulphinylbutyl‐ITC (sulforaphane). Apoptosis was determined by analysis of DNA content, annexin V staining, gel electrophoresis, CPP32 expression/inhibition and the histological appearance of nuclei. In terms of their ability to reduce adherent cell number, the relative potency of ITCs was BITC = AITC > PEITC ≫ sulforaphane. Non‐adherent cells from test flasks showed less evidence of apoptosis than those grown under control conditions. Our results implied that ITCs first blocked cells at G2/M and subsequently caused a loss in adherence which was not reduced by caspase inhibitors or by pre‐loading the cells with an antioxidant, the GST mimic Ebselen. This suggests that the primary action of ITCs is to block rapidly proliferating cancer cells in G2/M. In this particular p53 null cell line, loss of cell adherence was not part of an apoptotic process, nor did it involve free radical signaling pathways. © 2001 Society of Chemical Industry.