| Selective killing of oncogenically transformed cells through a ROS-mediated mechanism by beta-phenylethyl isothiocyanate. | |
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MedLine Citation:
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PMID: 16959615 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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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:
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Title: Cancer cell Volume: 10 ISSN: 1535-6108 ISO Abbreviation: Cancer Cell Publication Date: 2006 Sep |
Date Detail:
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Created Date: 2006-09-08 Completed Date: 2006-10-24 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 101130617 Medline TA: Cancer Cell Country: United States |
Other Details:
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Languages: eng Pagination: 241-52 Citation Subset: IM |
Affiliation:
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Department of Molecular Pathology, The University of Texas M.D. Anderson Cancer Center, Houston, Texas 77030, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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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:
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CA085563/CA/NCI NIH HHS; CA100428/CA/NCI NIH HHS; CA109041/CA/NCI NIH HHS; CA16672/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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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:
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Cancer Cell. 2006 Sep;10(3):175-6
[PMID:
16959608
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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