Journal of Zhejiang University SCIENCE  B

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Aurora kinase B in non-small cell lung cancer: molecular mechanisms, therapeutic resistance, and targeted therapies


Author(s):  Lin ZHAO1, Linrui MA1, Taoli ZHONG1, Zixuan WANG1, Xin LIN1, Huihui CHEN1, 2, Wei SONG1, 3, 4, Ziqing LIN1, Bingxin SUI5, Guangtao PAN1, Peiyu YAN6, 7

Affiliation(s):  1Faculty of Chinese Medicine, Macau University of Science and Technology, Macau 999078, China; more

Corresponding email(s):  pyyan@must.edu.mo, panguangtaowuhan@foxmail.com

Key Words:  Aurora kinase B (AURKB), Non-small cell lung cancer, Chromosomal instability, therapeutic resistance, Epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) resistance, Precision oncology, Aurora kinase inhibitor


Lin ZHAO1, Linrui MA1, Taoli ZHONG1, Zixuan WANG1, Xin LIN1, Huihui CHEN1,2, Wei SONG1,3,4, Ziqing LIN1, Bingxin SUI5, Guangtao PAN1, Peiyu YAN6,7. Aurora kinase B in non-small cell lung cancer: molecular mechanisms, therapeutic resistance, and targeted therapies[J]. Journal of Zhejiang University Science B,in press.Frontiers of Information Technology & Electronic Engineering,in press.https://doi.org/10.1631/jzus.B2600403

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author="Lin ZHAO1, Linrui MA1, Taoli ZHONG1, Zixuan WANG1, Xin LIN1, Huihui CHEN1,2, Wei SONG1,3,4, Ziqing LIN1, Bingxin SUI5, Guangtao PAN1, Peiyu YAN6,7",
journal="Journal of Zhejiang University Science B",
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publisher="Zhejiang University Press & Springer",
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%A Lin ZHAO1
%A Linrui MA1
%A Taoli ZHONG1
%A Zixuan WANG1
%A Xin LIN1
%A Huihui CHEN1
%A 2
%A Wei SONG1
%A 3
%A 4
%A Ziqing LIN1
%A Bingxin SUI5
%A Guangtao PAN1
%A Peiyu YAN6
%A 7
%J Journal of Zhejiang University SCIENCE B
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A1 - Lin ZHAO1
A1 - Linrui MA1
A1 - Taoli ZHONG1
A1 - Zixuan WANG1
A1 - Xin LIN1
A1 - Huihui CHEN1
A1 - 2
A1 - Wei SONG1
A1 - 3
A1 - 4
A1 - Ziqing LIN1
A1 - Bingxin SUI5
A1 - Guangtao PAN1
A1 - Peiyu YAN6
A1 - 7
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doi="https://doi.org/10.1631/jzus.B2600403"


Abstract: Non-small cell lung cancer (NSCLC) remains the leading cause of cancer-related mortality worldwide, and therapeutic resistance continues to be a major barrier to achieving durable clinical benefit. Increasing evidence has identified Aurora kinase B (AURKB), a key catalytic component of the chromosomal passenger complex (CPC), as an essential regulator of mitosis, chromosome segregation, and chromosomal instability (CIN) in NSCLC. Elevated AURKB expression or excessive AURKB signaling is closely associated with increased tumor proliferation, epithelial-mesenchymal transition (EMT), metastatic progression, and poor clinical outcomes. Mechanistically, AURKB interacts with multiple oncogenic signaling networks, including MYC, PI3K/AKT, MAPK, KRAS, and p53-related pathways, thereby promoting mitotic adaptation, survival under therapeutic stress, and tumor evolutionary plasticity. Accumulating evidence suggests that AURKB contributes to resistance to chemotherapy and epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) in NSCLC, partly by suppressing apoptosis, inducing mitotic slippage, and enhancing CIN-driven tumor heterogeneity. In this review, we comprehensively summarize the molecular structure, biological functions, and regulatory mechanisms of AURKB in NSCLC. We further discuss its oncogenic roles in tumor progression, EMT, metastasis, and therapeutic resistance, with particular emphasis on EGFR-TKI resistance and KRAS-driven lung cancer. We also discuss current challenges in the clinical translation of AURKB inhibitors and future biomarker-guided therapeutic strategies. Collectively, current evidence indicates that AURKB is a biologically and clinically relevant therapeutic target with promising translational potential in NSCLC.

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On-line Access: 2026-10-12

Received: 2026-07-07

Revision Accepted: 2026-09-18

Crosschecked: 0000-00-00

Cited: 0

Clicked: 111

Citations:  Bibtex RefMan EndNote GB/T7714

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