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SMARCA4-inactivating mutations increase sensitivity to Aurora kinase A inhibitor VX-680 in non-small cell lung cancers
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SMARCA4-inactivating mutations increase sensitivity to Aurora kinase A inhibitor VX-680 in non-small cell lung cancers
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Journal Article
SMARCA4-inactivating mutations increase sensitivity to Aurora kinase A inhibitor VX-680 in non-small cell lung cancers
2017
Overview
Mutations in the
SMARCA4/BRG1
gene resulting in complete loss of its protein (BRG1) occur frequently in non-small cell lung cancer (NSCLC) cells. Currently, no single therapeutic agent has been identified as synthetically lethal with SMARCA4/BRG1 loss. We identify AURKA activity as essential in NSCLC cells lacking SMARCA4/BRG1. In these cells, RNAi-mediated depletion or chemical inhibition of AURKA induces apoptosis and cell death
in vitro
and in xenograft mouse models. Disc large homologue-associated protein 5 (HURP/DLGAP5), required for AURKA-dependent, centrosome-independent mitotic spindle assembly is essential for the survival and proliferation of
SMARCA4/BRG1
mutant but not of
SMARCA4/BRG1
wild-type cells. AURKA inhibitors may provide a therapeutic strategy for biomarker-driven clinical studies to treat the NSCLCs harbouring
SMARCA4/BRG1
-inactivating mutations.
Lung cancers often harbour loss-of-function mutations in
SMARCA4
. Here, the authors demonstrate a vulnerability of
SMARCA4
-deficient lung cancers for Aurora kinase A inhibition associated with mitotic defects.
Publisher
Nature Publishing Group UK,Nature Publishing Group,Nature Portfolio
Subject
/ 38/23
/ 38/39
/ 38/47
/ 38/89
/ 38/91
/ 42/44
/ 631/67
/ Animals
/ Aurora Kinase A - antagonists & inhibitors
/ Aurora Kinase A - metabolism
/ Carcinoma, Non-Small-Cell Lung - drug therapy
/ Carcinoma, Non-Small-Cell Lung - genetics
/ Cells
/ Female
/ Gene Expression Regulation, Neoplastic
/ Genes
/ Genome-Wide Association Study
/ Genomes
/ Genomics
/ High-Throughput Nucleotide Sequencing
/ Humanities and Social Sciences
/ Humans
/ Kinases
/ Lung Neoplasms - drug therapy
/ Mice
/ Mutation
/ Nuclear Proteins - metabolism
/ Oncology
/ Protein Kinase Inhibitors - pharmacology
/ Proteins
/ Science
/ Transcription Factors - genetics
/ Transcription Factors - metabolism
/ Tumors
