Targeting Aurora B kinase prevents and overcomes resistance to EGFR inhibitors in lung cancer by enhancing BIM- and PUMA-mediated apoptosis.

Publication Type Academic Article
Authors Tanaka K, Yu H, Yang S, Han S, Selcuklu S, Kim K, Ramani S, Ganesan Y, Moyer A, Sinha S, Xie Y, Ishizawa K, Osmanbeyoglu H, Lyu Y, Roper N, Guha U, Rudin C, Kris M, Hsieh J, Cheng E
Journal Cancer Cell
Volume 39
Issue 9
Pagination 1245-1261.e6
Date Published 08/12/2021
ISSN 1878-3686
Keywords Acrylamides, Aniline Compounds, Carcinoma, Non-Small-Cell Lung, Drug Resistance, Neoplasm, Lung Neoplasms, Protein Kinase Inhibitors
Abstract The clinical success of EGFR inhibitors in EGFR-mutant lung cancer is limited by the eventual development of acquired resistance. We hypothesize that enhancing apoptosis through combination therapies can eradicate cancer cells and reduce the emergence of drug-tolerant persisters. Through high-throughput screening of a custom library of ∼1,000 compounds, we discover Aurora B kinase inhibitors as potent enhancers of osimertinib-induced apoptosis. Mechanistically, Aurora B inhibition stabilizes BIM through reduced Ser87 phosphorylation, and transactivates PUMA through FOXO1/3. Importantly, osimertinib resistance caused by epithelial-mesenchymal transition (EMT) activates the ATR-CHK1-Aurora B signaling cascade and thereby engenders hypersensitivity to respective kinase inhibitors by activating BIM-mediated mitotic catastrophe. Combined inhibition of EGFR and Aurora B not only efficiently eliminates cancer cells but also overcomes resistance beyond EMT.
DOI 10.1016/j.ccell.2021.07.006
PubMed ID 34388376
PubMed Central ID PMC8440494
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