ArticleNature communications2019
AURKB as a target in non-small cell lung cancer with acquired resistance to anti-EGFR therapy.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 79 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
79 citing papers in PubMed, 146 citations in OpenAlex.
- Review
- AURKB-mediated phosphorylation of metabolic enzyme CD73 drives immune suppression and renal cell carcinoma progression.Cell death and differentiation · 2026Article
- Mitotic Machinery Dysregulation in Lung Cancer: Biological Roles, Therapeutic Targeting, and Combination Strategies.Pharmaceutics · 2026Review
- Article
- KRAS mutated lung adenocarcinoma responds to pan-ERBB and Aurora kinase inhibitors.NPJ precision oncology · 2026Article
- Targeting the SYVN1-EGFR axis: a breakthrough strategy for TKI-resistant NSCLC.Cell death & disease · 2025Article
- Benzaldehyde suppresses epithelial-mesenchymal plasticity and overcomes treatment resistance in cancer by targeting the interaction of 14-3-3ζ with H3S28ph.British journal of cancer · 2025Article
- Article
- AURKB inhibition induces rhabdomyosarcoma apoptosis and ferroptosis through NPM1/SP1/ACSL5 axis.JCI insight · 2025Article
- EHMT2-mediated R-loop formation promotes the malignant progression of prostate cancer via activating Aurora B.Clinical and translational medicine · 2025Article
- [High expression of AURKB promotes malignant phenotype of osteosarcoma cells by activating nuclear factor-κB signalingNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- AURKB promotes immunogenicity and immune infiltration in clear cell renal cell carcinoma.Discover oncology · 2024Article
- Article
- Quantifying Landscape-Flux via Single-Cell Transcriptomics Uncovers the Underlying Mechanism of Cell Cycle.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Article
- Design, synthesis, and evaluation of dual EGFR/AURKB inhibitors as anticancer agents for non-small cell lung cancer.Bioorganic & medicinal chemistry letters · 2024Article
- Clinical translation for targeting DNA damage repair in non-small cell lung cancer: a review.Translational lung cancer research · 2024Review
- Construction of a hepatocytes-related and protein kinase-related gene signature in HCC based on ScRNA-Seq analysis and machine learning algorithm.Journal of physiology and biochemistry · 2023Article
- The effect of PLK1 inhibitor in osimertinib resistant non-small cell lung carcinoma cells.Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2023Article
- Signature-driven repurposing of Midostaurin for combination with MEK1/2 and KRASG12C inhibitors in lung cancer.Nature communications · 2023Article
19 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Non-small cell lung cancer (NSCLC) tumors harboring mutations in EGFR ultimately relapse to therapy with EGFR tyrosine kinase inhibitors (EGFR TKIs). Here, we show that resistant cells without the p.T790M or other acquired mutations are sensitive to the Aurora B (AURKB) inhibitors barasertib and S49076. Phospho-histone H3 (pH3), a major product of AURKB, is increased in most resistant cells and treatment with AURKB inhibitors reduces the levels of pH3, triggering G1/S arrest and polyploidy. Senescence is subsequently induced in cells with acquired mutations while, in their absence, polyploidy is followed by cell death. Finally, in NSCLC patients, pH3 levels are increased after progression on EGFR TKIs and high pH3 baseline correlates with shorter survival. Our results reveal that AURKB activation is associated with acquired resistance to EGFR TKIs, and that AURKB constitutes a potential target in NSCLC progressing to anti-EGFR therapy and not carrying resistance mutations.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.