Title of article :
Selective killing of oncogenically transformed cells through a ROS-mediated mechanism by β-phenylethyl isothiocyanate
Author/Authors :
Trachootham، نويسنده , , Dunyaporn and Zhou، نويسنده , , Yan and Zhang، نويسنده , , Hui and Demizu، نويسنده , , Yusuke and Chen، نويسنده , , Zhao and Pelicano، نويسنده , , Helene and Chiao، نويسنده , , Paul J. and Achanta، نويسنده , , Geetha and Arlinghaus، نويسنده , , Ralph B. and Liu، نويسنده , , Jinsong and Huang، نويسنده , , Peng، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2006
Pages :
12
From page :
241
To page :
252
Abstract :
Summary ve 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 β-phenylethyl isothiocyanate (PEITC). Oncogenic transformation of ovarian epithelial cells with H-RasV12 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.
Keywords :
CELLCYCLE
Journal title :
Cancer Cell
Serial Year :
2006
Journal title :
Cancer Cell
Record number :
1335763
Link To Document :
بازگشت