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PMID: 15753404 Published · ppublish English Journal Article Research Support, U.S. Gov't, P.H.S.

Bax and Bak are required for apoptosis induction by sulforaphane, a cruciferous vegetable-derived cancer chemopreventive agent.

Cancer research ·Vol. 65 ·No. 5 ·2005-03-01 ·Pages 2035-43

Choi S, Singh SV

Abstract

Sulforaphane, a constituent of many edible cruciferous vegetables, including broccoli, effectively suppresses proliferation of cancer cells in culture and in vivo by causing apoptosis induction, but the sequence of events leading to cell death is poorly defined. Here, we show that multidomain proapoptotic Bcl-2 family members Bax and Bak play a critical role in apoptosis induction by sulforaphane. This conclusion is based on the following observations: (a) sulforaphane treatment caused a dose- and time-dependent increase in the protein levels of both Bax and Bak and conformational change and mitochondrial translocation of Bax in SV40-transformed mouse embryonic fibroblasts (MEF) derived from wild-type mice to trigger cytosolic release of apoptogenic molecules (cytochrome c and Smac/DIABLO), activation of caspase-9 and caspase-3, and ultimately cell death; (b) MEFs derived from Bax or Bak knockout mice resisted cell death by sulforaphane, and (c) MEFs derived from Bax and Bak double knockout mice exhibited even greater protection against sulforaphane-induced cytochrome c release, caspase activation, and apoptosis compared with wild-type or single knockout cells. Interestingly, sulforaphane treatment also caused a dose- and time-dependent increase in the protein level of Apaf-1 in wild-type, Bax-/-, and Bak-/- MEFs but not in double knockout, suggesting that Bax and Bak might regulate sulforaphane-mediated induction of Apaf-1 protein. A marked decline in the protein level of X-linked inhibitor of apoptosis on treatment with sulforaphane was also observed. Thus, it is reasonable to postulate that sulforaphane-induced apoptosis is amplified by a decrease in X-linked inhibitor of apoptosis level, which functions to block cell death by inhibiting activities of caspases. In conclusion, the results of the present study indicate that Bax and Bak proteins play a critical role in initiation of cell death by sulforaphane.

MeSH Terms
Animals Anticarcinogenic Agents/pharmacology Apoptosis Apoptosis Regulatory Proteins Apoptotic Protease-Activating Factor 1 Carrier Proteins/metabolism Caspase 3 Caspase 9 Caspases/metabolism Cell Proliferation/drug effects Cells, Cultured Chemoprevention Complement Membrane Attack Complex Complement System Proteins Cytochromes c/metabolism Enzyme Activation Epithelial Cells Fibroblasts/drug effects,metabolism Glycoproteins/metabolism Isothiocyanates Male Membrane Proteins/metabolism Mice Mice, Knockout Mitochondria/drug effects Mitochondrial Proteins/metabolism Prostate/metabolism Prostatic Neoplasms/metabolism,pathology Protein Conformation/drug effects Protein Transport Proteins/metabolism Proto-Oncogene Proteins c-bcl-2/metabolism Sulfoxides Thiocyanates/pharmacology bcl-2 Homologous Antagonist-Killer Protein bcl-2-Associated X Protein
Chemicals
Anticarcinogenic Agents Apaf1 protein, mouse Apoptosis Regulatory Proteins Apoptotic Protease-Activating Factor 1 Bak1 protein, mouse Bax protein, mouse Carrier Proteins Complement Membrane Attack Complex Diablo protein, mouse Glycoproteins Isothiocyanates Membrane Proteins Mitochondrial Proteins Proteins Proto-Oncogene Proteins c-bcl-2 SC5b-9 protein complex Sulfoxides Thiocyanates bcl-2 Homologous Antagonist-Killer Protein bcl-2-Associated X Protein Complement System Proteins Cytochromes c Casp3 protein, mouse Casp9 protein, mouse Caspase 3 Caspase 9 Caspases sulforaphane
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Choi Sunga
Department of Pharmacology and University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213, USA.
Singh Shivendra V
Article Info
Journal
Cancer research
Abbr.
Cancer Res
ISSN
0008-5472
Published
2005-03-01
Pages
2035-43
Language
English
Region
United States
NLM ID
2984705R
Subset
IM
Grants
NCI NIH HHS · CA076348 · United States
NCI NIH HHS · CA101753 · United States
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