Abstract
The three human RAS proteins are mutated and constitutively activated in ∼20% of cancers leading to cell growth and proliferation. For the past three decades, many attempts have been made to inhibit these proteins with little success. Recently; however, multiple methods have emerged to inhibit KRAS, the most prevalently mutated isoform. These methods and the underlying biology will be discussed in this review with a special focus on KRAS-plasma membrane interactions.
Keywords:
RAS; cancer; phospholipids; plasma membrane; small molecule inhibitors; therapeutics.
© 2020 The Author(s). Published by Portland Press Limited on behalf of the Biochemical Society.
Publication types
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Research Support, N.I.H., Extramural
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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 / pharmacology*
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Cell Membrane / metabolism*
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Humans
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Molecular Targeted Therapy
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Mutation
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Neoplasms / genetics*
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Neoplasms / metabolism
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Protein Isoforms
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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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ras Proteins / chemistry
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ras Proteins / genetics
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ras Proteins / metabolism*
Substances
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Antineoplastic Agents
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KRAS protein, human
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Protein Isoforms
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Proto-Oncogene Proteins p21(ras)
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ras Proteins