Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential.

Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential. Research Abstract Details 

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Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential. Abstract Text:

Dong Xiao,Karen L Lew,Yan Zeng,Hui Xiao,Stanley W Marynowski,Rajiv Dhir,Shivendra V Singh,

The present study was undertaken to gain insights into the molecular mechanism of apoptosis induction by phenethyl isothiocyanate (PEITC), which is a cancer chemopreventive constituent of cruciferous vegetables, using PC-3 human prostate cancer cells as a model. The PEITC-induced cell death in PC-3 cells was associated with disruption of the mitochondrial membrane potential, release of apoptogenic molecules (cytochrome c and Smac/DIABLO) from mitochondria to the cytosol and generation of reactive oxygen species (ROS), which were blocked in the presence of a combined mimetic of superoxide dismutase and catalase (Euk134). Ectopic expression of Bcl-xL, whose protein level is reduced markedly on treatment of PC-3 cells with PEITC, conferred partial protection against PEITC-induced apoptosis only at higher drug concentrations (>10 microM). Administration of 12 micromol PEITC/day (Monday through Friday) by oral gavage significantly retarded growth of PC-3 xenografts in athymic mice. For instance, 31 days after the initiation of PEITC administration, the average tumor volume in control mice (721 +/- 153 mm3) was approximately 2-fold higher compared with mice receiving 12 micromol PEITC/day. The PEITC-mediated inhibition of PC-3 xenograft growth was associated with induction of Bax and Bid proteins. In conclusion, the present study indicates that the PEITC-induced apoptosis in PC-3 cells is mediated by ROS-dependent disruption of the mitochondrial membrane potential and regulated by Bax and Bid.

Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential. Publishing Authors By Initials

D Xiao,KL Lew,Y Zeng,H Xiao,SW Marynowski,R Dhir,SV Singh,

For similar peptides: intracellular signaling peptides and proteins: apoptosis regulatory proteins: proto-oncogene proteins c-bcl-2: bcl-2-associated x protein research abstracts see: peptides: intracellular signaling peptides and proteins: apoptosis regulatory proteins: proto-oncogene proteins c-bcl-2: bcl-2-associated x protein research

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Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Carcinogenesis

VOLUME: 27

Page Numbers: 2223-34

Journal Abbreviation: Carcinogenesis

ISSN: 0143-3334

DAY: 13

MONTH: 06

YEAR: 2006

Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8008055

Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential. Keywords Mesh Terms:

KEYWORDS: bcl-2-Associated X Protein

MESH TERMS: metabolism

Chemical & Substance for Abstract: Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential. Information

Substance Name: phenethyl isothiocyanate

Registry Number: 2257-09-2

Grant and Affiliation Information for Phenethyl isothiocyanate-induced apoptosis in PC-3 human prostate cancer cells is mediated by reactive oxygen species-dependent disruption of the mitochondrial membrane potential.

AFFILIATION: Department of Pharmacology and University of Pittsburgh Cancer Institute, University of Pittsburgh School of Medicine Pittsburgh, PA, USA.

Country: England

AGENCY: United States NCI

GRANT: CA115498

ACRONYM: CA

MEDLINETA: Carcinogenesis

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