TY - JOUR
T1 - The two faces of reactive oxygen species in cancer
AU - Reczek, Colleen R.
AU - Chandel, Navdeep S.
N1 - Funding Information:
This work was supported by a National Cancer Institute grant (RO1 CA123067-09) to N.S.C. C.R.R. was supported by a National Institutes of Health postdoctoral training grant (T32 HL076139-11). The authors apologize for any references left uncited due to space limitations.
Publisher Copyright:
© 2017 by Annual Reviews. All rights reserve.
PY - 2017
Y1 - 2017
N2 - Reactive oxygen species (ROS), now appreciated for their cellular signaling capabilities, have a dual role in cancer. On the one hand, ROS can promote protumorigenic signaling, facilitating cancer cell proliferation, survival, and adaptation to hypoxia. On the other hand, ROS can promote antitumorigenic signaling and trigger oxidative stress-induced cancer cell death. To hyperactivate the cell signaling pathways necessary for cellular transformation and tumorigenesis, cancer cells increase their rate of ROS production compared with normal cells. Concomitantly, in order to maintain ROS homeostasis and evade cell death, cancer cells increase their antioxidant capacity. Compared with normal cells, this altered redox environment of cancer cells may increase their susceptibility to ROS-manipulation therapies. In this review, we discuss the two faces of ROS in cancer, the potential mechanisms underlying ROS signaling, and the opposing cancer therapeutic approaches to targeting ROS.
AB - Reactive oxygen species (ROS), now appreciated for their cellular signaling capabilities, have a dual role in cancer. On the one hand, ROS can promote protumorigenic signaling, facilitating cancer cell proliferation, survival, and adaptation to hypoxia. On the other hand, ROS can promote antitumorigenic signaling and trigger oxidative stress-induced cancer cell death. To hyperactivate the cell signaling pathways necessary for cellular transformation and tumorigenesis, cancer cells increase their rate of ROS production compared with normal cells. Concomitantly, in order to maintain ROS homeostasis and evade cell death, cancer cells increase their antioxidant capacity. Compared with normal cells, this altered redox environment of cancer cells may increase their susceptibility to ROS-manipulation therapies. In this review, we discuss the two faces of ROS in cancer, the potential mechanisms underlying ROS signaling, and the opposing cancer therapeutic approaches to targeting ROS.
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U2 - 10.1146/annurev-cancerbio-041916-065808
DO - 10.1146/annurev-cancerbio-041916-065808
M3 - Article
AN - SCOPUS:85022342206
SN - 2472-3428
VL - 1
SP - 79
EP - 98
JO - Annual Review of Cancer Biology
JF - Annual Review of Cancer Biology
ER -
