TY - JOUR
T1 - Targeting cancer cells by ROS-mediated mechanisms
T2 - A radical therapeutic approach?
AU - Trachootham, Dunyaporn
AU - Alexandre, Jerome
AU - Huang, Peng
N1 - Funding Information:
Contributions to the scientific reports cited in this work were supported in part by grants CA085563, CA100428 and CA109041 to P.H. from the National Institutes of Health and a research grant from the CLL global research foundation. D.T. is a recipient of a scholarship from the Anandamahidol Foundation under the royal patronage of His Majesty the King of Thailand, and a recipient of the Lummis Family Fellowship in Biomedical Sciences.
PY - 2009
Y1 - 2009
N2 - Increased generation of reactive oxygen species (ROS) and an altered redox status have long been observed in cancer cells, and recent studies suggest that this biochemical property of cancer cells can be exploited for therapeutic benefits. Cancer cells in advanced stage tumours frequently exhibit multiple genetic alterations and high oxidative stress, suggesting that it might be possible to preferentially eliminate these cells by pharmacological ROS insults. However, the upregulation of antioxidant capacity in adaptation to intrinsic oxidative stress in cancer cells can confer drug resistance. Abrogation of such drug-resistant mechanisms by redox modulation could have significant therapeutic implications. We argue that modulating the unique redox regulatory mechanisms of cancer cells might be an effective strategy to eliminate these cells.
AB - Increased generation of reactive oxygen species (ROS) and an altered redox status have long been observed in cancer cells, and recent studies suggest that this biochemical property of cancer cells can be exploited for therapeutic benefits. Cancer cells in advanced stage tumours frequently exhibit multiple genetic alterations and high oxidative stress, suggesting that it might be possible to preferentially eliminate these cells by pharmacological ROS insults. However, the upregulation of antioxidant capacity in adaptation to intrinsic oxidative stress in cancer cells can confer drug resistance. Abrogation of such drug-resistant mechanisms by redox modulation could have significant therapeutic implications. We argue that modulating the unique redox regulatory mechanisms of cancer cells might be an effective strategy to eliminate these cells.
UR - http://www.scopus.com/inward/record.url?scp=67650071137&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=67650071137&partnerID=8YFLogxK
U2 - 10.1038/nrd2803
DO - 10.1038/nrd2803
M3 - Review article
C2 - 19478820
AN - SCOPUS:67650071137
SN - 1474-1776
VL - 8
SP - 579
EP - 591
JO - Nature Reviews Drug Discovery
JF - Nature Reviews Drug Discovery
IS - 7
ER -