Abstract
Celastrol binds CIP2A and enhances CIP2A-CHIP interaction, leading to ubiquitination/degradation of CIP2A and inhibition of lung cancer cells in vitro and in vivo. Celastrol potentiates cisplatin's efficacy by suppressing the CIP2A-Akt pathway, and therefore CIP2A inhibitors may represent novel therapeutics for cancer.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Autoantigens / drug effects*
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Autoantigens / metabolism
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Biomarkers, Tumor / metabolism*
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Carcinoma, Non-Small-Cell Lung / enzymology
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Carcinoma, Non-Small-Cell Lung / metabolism*
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Carcinoma, Non-Small-Cell Lung / pathology
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Cell Line, Tumor
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Humans
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Intracellular Signaling Peptides and Proteins
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Lung Neoplasms / enzymology
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Lung Neoplasms / metabolism*
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Lung Neoplasms / pathology
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Membrane Proteins / drug effects*
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Membrane Proteins / metabolism
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Mice
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Pentacyclic Triterpenes
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Proteolysis
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Triterpenes / pharmacology*
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Ubiquitination
Substances
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Autoantigens
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Biomarkers, Tumor
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CIP2A protein, human
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Intracellular Signaling Peptides and Proteins
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Membrane Proteins
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Pentacyclic Triterpenes
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Triterpenes
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celastrol