@article{04e81c49980c47f3897343b4c18995e0,
title = "Redox regulation in cancer cells during metastasis",
abstract = "Metastasis is an inefficient process in which the vast majority of cancer cells are fated to die, partly because they experience oxidative stress. Metastasizing cancer cells migrate through diverse environments that differ dramatically from their tumor of origin, leading to redox imbalances. The rare metastasizing cells that survive undergo reversible metabolic changes that confer oxidative stress resistance. We review the changes in redox regulation that cancer cells undergo during metastasis. By better understanding these mechanisms, it may be possible to develop pro-oxidant therapies that block disease progression by exacerbating oxidative stress in cancer cells. Significance: Oxidative stress often limits cancer cell survival during metastasis, raising the possibility of inhibiting cancer progression with pro-oxidant therapies. This is the opposite strategy of treating patients with antioxidants, an approach that worsened outcomes in large clinical trials.",
author = "Alpaslan Tasdogan and Ubellacker, {Jessalyn M.} and Morrison, {Sean J.}",
note = "Funding Information: S.J. Morrison is a Howard Hughes Medical Institute 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. This work was supported by the Cancer Prevention and Research Institute of Texas (RP170114 and RP180778) and by the NIH (U01 CA228608). A. Tasdogan was supported by the Leopoldina Fellow-ship (LPDS 2016-16) from the German National Academy of Sci-ences and the Fritz Thyssen Foundation. All figures were generated using BioRender (paid license). Funding Information: S.J. Morrison is a Howard Hughes Medical Institute 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. This work was supported by the Cancer Prevention and Research Institute of Texas (RP170114 and RP180778) and by the NIH (U01 CA228608). A. Tasdogan was supported by the Leopoldina Fellowship (LPDS 2016-16) from the German National Academy of Sciences and the Fritz Thyssen Foundation. All figures were generated using BioRender (paid license). Publisher Copyright: {\textcopyright} 2021 The Authors.",
year = "2021",
month = nov,
doi = "10.1158/2159-8290.CD-21-0558",
language = "English (US)",
volume = "11",
pages = "2682--2692",
journal = "Cancer Discovery",
issn = "2159-8274",
publisher = "American Association for Cancer Research Inc.",
number = "11",
}