TY - JOUR
T1 - Cancer, oxidative stress, and metastasis
AU - Gill, Jennifer G.
AU - Piskounova, Elena
AU - Morrison, Sean J.
N1 - Funding Information:
S.J.M. is a Howard Hughes Medical Institute (HHMI) Investigator, the Mary McDermott Cook Chair in Pediatric Genetics, the Kathryn and Gene Bishop Distinguished Chair in Pediatric Research, the director of the Hamon Laboratory for Stem Cells and Cancer, and a Cancer Prevention and Research Institute of Texas Scholar. We thank Alpaslan Tasdogan and Kati Ahlqvist for discussion and critical comments. This work was supported by the Cancer Prevention and Research Institute of Texas and the National Institutes of Health (R37 AG024945 and R01 DK100848).
Publisher Copyright:
© 2016 Gill et al.
PY - 2016
Y1 - 2016
N2 - Reactive oxygen species (ROS) are highly reactive molecules that arise from a number of cellular sources, including oxidative metabolism in mitochondria. At low levels they can be advantageous to cells, activating signaling pathways that promote proliferation or survival. At higher levels, ROS can damage or kill cells by oxidizing proteins, lipids, and nucleic acids. It was hypothesized that antioxidants might benefit high-risk patients by reducing the rate of ROS-induced mutations and delaying cancer initiation. However, dietary supplementation with antioxidants has generally proven ineffective or detrimental in clinical trials. High ROS levels limit cancer cell survival during certain windows of cancer initiation and progression. During these periods, dietary supplementation with antioxidants may promote cancer cell survival and cancer progression. This raises the possibility that rather than treating cancer patients with antioxidants, they should be treated with pro-oxidants that exacerbate oxidative stress or block metabolic adaptations that confer oxidative stress resistance.
AB - Reactive oxygen species (ROS) are highly reactive molecules that arise from a number of cellular sources, including oxidative metabolism in mitochondria. At low levels they can be advantageous to cells, activating signaling pathways that promote proliferation or survival. At higher levels, ROS can damage or kill cells by oxidizing proteins, lipids, and nucleic acids. It was hypothesized that antioxidants might benefit high-risk patients by reducing the rate of ROS-induced mutations and delaying cancer initiation. However, dietary supplementation with antioxidants has generally proven ineffective or detrimental in clinical trials. High ROS levels limit cancer cell survival during certain windows of cancer initiation and progression. During these periods, dietary supplementation with antioxidants may promote cancer cell survival and cancer progression. This raises the possibility that rather than treating cancer patients with antioxidants, they should be treated with pro-oxidants that exacerbate oxidative stress or block metabolic adaptations that confer oxidative stress resistance.
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U2 - 10.1101/sqb.2016.81.030791
DO - 10.1101/sqb.2016.81.030791
M3 - Article
C2 - 28082378
AN - SCOPUS:85021042620
SN - 0091-7451
VL - 81
SP - 163
EP - 175
JO - Cold Spring Harbor Symposia on Quantitative Biology
JF - Cold Spring Harbor Symposia on Quantitative Biology
IS - 1
ER -