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Relapse-associated AURKB blunts the glucocorticoid sensitivity of B cell acute lymphoblastic leukemia
Journal article   Open access   Peer reviewed

Relapse-associated AURKB blunts the glucocorticoid sensitivity of B cell acute lymphoblastic leukemia

Coralie Poulard, Hye Na Kim, Mimi Fang, Karina Kruth, Celine Gagnieux, Daniel S Gerke, Deepa Bhojwani, Yong-Mi Kim, Martin Kampmann, Michael R Stallcup, …
Proceedings of the National Academy of Sciences - PNAS, Vol.116(8), pp.3052-3061
02/19/2019
DOI: 10.1073/pnas.1816254116
PMCID: PMC6386662
PMID: 30733284
url
https://europepmc.org/articles/pmc6386662View
Published (Version of record) Open Access

Abstract

Glucocorticoids (GCs) are used in combination chemotherapies as front-line treatment for B cell acute lymphoblastic leukemia (B-ALL). Although effective, many patients relapse and become resistant to chemotherapy and GCs in particular. Why these patients relapse is not clear. We took a comprehensive, functional genomics approach to identify sources of GC resistance. A genome-wide shRNA screen identified the transcriptional coactivators EHMT2, EHMT1, and CBX3 as important contributors to GC-induced cell death. This complex selectively supports GC-induced expression of genes contributing to cell death. A metaanalysis of gene expression data from B-ALL patient specimens revealed that Aurora kinase B (AURKB), which restrains GC signaling by phosphorylating EHMT1-2, is overexpressed in relapsed B-ALL, suggesting it as a potential contributor to relapse. Inhibition of AURKB enhanced GC-induced expression of cell death genes, resulting in potentiation of GC cytotoxicity in cell lines and relapsed B-ALL patient samples. This function for AURKB is distinct from its canonical role in the cell cycle. These results show the utility of functional genomics in understanding mechanisms of resistance and rapidly identifying combination chemotherapeutics.
Aurora Kinase B - genetics Cell Death - genetics Cell Line, Tumor Chromosomal Proteins, Non-Histone - genetics Drug Resistance, Neoplasm - genetics Gene Expression Regulation, Leukemic - genetics Glucocorticoids - genetics Glucocorticoids - pharmacology Histocompatibility Antigens - genetics Histone-Lysine N-Methyltransferase - genetics Humans Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - drug therapy Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - genetics Precursor B-Cell Lymphoblastic Leukemia-Lymphoma - pathology Recurrence RNA, Small Interfering - genetics

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