Cell death in the colorectal cancer cell line HT29 in response to glucosinolate metabolites
- 14 June 2001
- journal article
- research article
- Published by Wiley in Journal of the Science of Food and Agriculture
- Vol. 81 (9) , 959-961
- https://doi.org/10.1002/jsfa.904
Abstract
No abstract availableKeywords
This publication has 9 references indexed in Scilit:
- Molecular mechanism of rapid cellular accumulation of anticarcinogenic isothiocyanatesCarcinogenesis: Integrative Cancer Research, 2001
- Role of glutathione in the accumulation of anticarcinogenic isothiocyanates and their glutathione conjugates by murine hepatoma cellsCarcinogenesis: Integrative Cancer Research, 2000
- Studies on the mechanism of the inhibition of human leukaemia cell growth by dietary isothiocyanates and their cysteine adducts in vitroBiochemical Pharmacology, 2000
- Apoptosis can be detected in attached colonic adenocarcinoma HT29 cells using annexin V binding, but not by TUNEL assay or sub-G0 DNA contentCytometry, 2000
- Selective increase of the potential anticarcinogen 4- methylsulphinylbutyl glucosinolate in broccoliCarcinogenesis: Integrative Cancer Research, 1998
- Inhibition of dimethylhydrazine-induced aberrant crypt foci and induction of apoptosis in rat colon following oral administration of the glucosinolate sinigrinCarcinogenesis: Integrative Cancer Research, 1998
- Molecular Mechanisms of c-Jun N-terminal Kinase-mediated Apoptosis Induced by Anticarcinogenic IsothiocyanatesJournal of Biological Chemistry, 1998
- Disruption of epithelial cell-matrix interactions induces apoptosisThe Journal of cell biology, 1994
- Isothiocyanates inhibit cell cycle progression of HeLa cells at G2/M phaseAnti-Cancer Drugs, 1993