Abstract
Oncogenic KRAS is one of the most common drivers of human cancer. Despite intense research, no effective therapy to directly inhibit oncogenic KRAS has yet been approved and KRAS mutant tumors remain associated with a poor prognosis. This short review discusses the current knowledge of the redox regulation of RAS and examines the newest findings on cysteine 118 (C118) as a potential novel target for KRAS inhibition.
Keywords:
Cysteine modification; RAS; Redox regulation.
Copyright © 2020 Elsevier Ltd. All rights reserved.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Antineoplastic Agents / therapeutic use*
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Cysteine / metabolism*
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Gene Expression Regulation, Neoplastic
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Humans
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Hydrogen Peroxide / therapeutic use
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Mutation
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Neoplasms / drug therapy
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Neoplasms / genetics
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Neoplasms / metabolism*
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Neoplasms / pathology
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Nitrosation
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Oxidation-Reduction / drug effects
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Piperazines / therapeutic use*
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Protease Inhibitors / therapeutic use
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Protein Processing, Post-Translational*
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Proto-Oncogene Proteins p21(ras) / antagonists & inhibitors
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Proto-Oncogene Proteins p21(ras) / genetics
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Proto-Oncogene Proteins p21(ras) / metabolism*
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Pyridines / therapeutic use*
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Pyrimidines / therapeutic use*
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Signal Transduction
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Sulfinic Acids
Substances
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Antineoplastic Agents
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KRAS protein, human
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Piperazines
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Protease Inhibitors
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Pyridines
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Pyrimidines
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Sulfinic Acids
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sotorasib
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Hydrogen Peroxide
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Proto-Oncogene Proteins p21(ras)
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Cysteine