Please use this identifier to cite or link to this item: https://doi.org/10.1016/j.redox.2018.101094
Title: gRASping the redox lever to modulate cancer cell fate signaling
Authors: Foo, C.H.J. 
Pervaiz, S. 
Keywords: Cancer
RAS
Reactive Oxygen Species
Issue Date: 2019
Publisher: Elsevier B.V.
Citation: Foo, C.H.J., Pervaiz, S. (2019). gRASping the redox lever to modulate cancer cell fate signaling. Redox Biology 25 : 101094. ScholarBank@NUS Repository. https://doi.org/10.1016/j.redox.2018.101094
Rights: Attribution-NonCommercial-NoDerivatives 4.0 International
Abstract: RAS proteins are critical regulators of signaling networks controlling diverse cellular functions such as cell proliferation and survival and its mutation are among the most powerful oncogenic drivers in human cancers. Despite intense efforts, direct RAS-targeting strategies remain elusive due to its “undruggable” nature. To that end, bulk of the research efforts has been directed towards targeting upstream and/or downstream of RAS signaling. However, the therapeutic efficacies of these treatments are limited in the long run due to the acquired drug resistance in RAS-driven cancers. Interestingly, recent studies have uncovered a potential role of RAS in redox-regulation as well as the interplay between ROS and RAS-associated signaling networks during process of cancer initiation and progression. More specifically, these studies provide ample evidence to implicate RAS as a redox-rheostat, manipulating ROS levels to provide a redox-milieu conducive for carcinogenesis. Importantly, the understanding of RAS-ROS interplay could provide us with novel targetable vulnerabilities for designing therapeutic strategies. In this review, we provide a brief summary of the advances in the field to illustrate the dual role of RAS in redox-regulation and its implications in RAS signaling outcomes and also emerging redox-based strategies to target RAS-driven cancers. © 2019 The Authors
Source Title: Redox Biology
URI: https://scholarbank.nus.edu.sg/handle/10635/209956
ISSN: 2213-2317
DOI: 10.1016/j.redox.2018.101094
Rights: Attribution-NonCommercial-NoDerivatives 4.0 International
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