Document Detail


Selective killing of oncogenically transformed cells through a ROS-mediated mechanism by beta-phenylethyl isothiocyanate.
MedLine Citation:
PMID:  16959615     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Reactive oxygen species (ROS) stimulate cell proliferation and induce genetic instability, and their increase in cancer cells is often viewed as an adverse event. Here, we show that such abnormal increases in ROS can be exploited to selectively kill cancer cells using beta-phenylethyl isothiocyanate (PEITC). Oncogenic transformation of ovarian epithelial cells with H-Ras(V12) or expression of Bcr-Abl in hematopoietic cells causes elevated ROS generation and renders the malignant cells highly sensitive to PEITC, which effectively disables the glutathione antioxidant system and causes severe ROS accumulation preferentially in the transformed cells due to their active ROS output. Excessive ROS causes oxidative mitochondrial damage, inactivation of redox-sensitive molecules, and massive cell death. In vivo, PEITC exhibits therapeutic activity and prolongs animal survival.
Authors:
Dunyaporn Trachootham; Yan Zhou; Hui Zhang; Yusuke Demizu; Zhao Chen; Helene Pelicano; Paul J Chiao; Geetha Achanta; Ralph B Arlinghaus; Jinsong Liu; Peng Huang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.    
Journal Detail:
Title:  Cancer cell     Volume:  10     ISSN:  1535-6108     ISO Abbreviation:  Cancer Cell     Publication Date:  2006 Sep 
Date Detail:
Created Date:  2006-09-08     Completed Date:  2006-10-24     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  101130617     Medline TA:  Cancer Cell     Country:  United States    
Other Details:
Languages:  eng     Pagination:  241-52     Citation Subset:  IM    
Affiliation:
Department of Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antioxidants / metabolism
Cell Death / drug effects
Cell Line
Cell Transformation, Neoplastic / genetics*
Fusion Proteins, bcr-abl / metabolism
Glutathione / metabolism
Humans
Isothiocyanates / pharmacology*,  therapeutic use
Mice
Neoplasms / drug therapy,  pathology
Oncogene Protein p21(ras) / genetics*,  metabolism*
Reactive Oxygen Species / metabolism*
Survival Rate
Xenograft Model Antitumor Assays
Grant Support
ID/Acronym/Agency:
CA085563/CA/NCI NIH HHS; CA100428/CA/NCI NIH HHS; CA109041/CA/NCI NIH HHS; CA16672/CA/NCI NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Fusion Proteins, bcr-abl; 0/Isothiocyanates; 0/Reactive Oxygen Species; 2257-09-2/phenethyl isothiocyanate; 70-18-8/Glutathione; EC 3.6.5.2/Oncogene Protein p21(ras)
Comments/Corrections
Comment In:
Cancer Cell. 2006 Sep;10(3):175-6   [PMID:  16959608 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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