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已发表论文
非小细胞肺癌中微小 RNA 调控 EGFR-TKI 耐药的复杂网络：综述
Received 24 July 2025
Accepted for publication 1 November 2025
Published 11 November 2025 Volume 2025:17 Pages 2729—2737
DOI https://doi.org/10.2147/CMAR.S555993
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 3
Editor who approved publication: Professor Seema Singh
Ying Xu,1,2 Jie Huang1
1Department of Thoracic Oncology, Hangzhou Cancer Hospital, Affiliated Hangzhou First People’s Hospital, Westlake University School of Medicine, Hangzhou, Zhejiang, People’s Republic of China; 2The Fourth School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, People’s Republic of China
Correspondence: Jie Huang, Email drhunter@aliyun.com
Abstract: Non-small cell lung cancer (NSCLC) harboring activating mutations in the Epidermal Growth Factor Receptor (EGFR) has been effectively treated with EGFR tyrosine kinase inhibitors (TKIs). However, the clinical efficacy of these targeted therapies is invariably limited by the development of acquired resistance. While secondary mutations like T790M and bypass pathway activation are well-documented mechanisms, there is a growing appreciation for the profound role of epigenetic regulators, particularly microRNAs (miRNAs), in orchestrating the resistant phenotype. This review provides a comprehensive and detailed analysis of the multifaceted roles of miRNAs in the emergence and maintenance of EGFR-TKI resistance in NSCLC, including their regulation of alternative receptor tyrosine kinase signaling pathways, driving phenotypic plasticity, specifically the epithelial-mesenchymal transition (EMT) and the acquisition of cancer stem cell (CSC) characteristics, as well as dysregulating core cellular processes, such as apoptosis. We further examine the complex interplay within competing endogenous RNA (ceRNA) networks, where long non-coding RNAs and circular RNAs sequester miRNAs, thereby modulating the expression of resistance-associated genes. Finally, the potential of specific miRNAs as circulating biomarkers for monitoring treatment response and as therapeutic targets to overcome resistance is discussed. This review underscores the central role of miRNA-mediated gene regulation as a critical layer of complexity in EGFR-TKI resistance, highlighting a sophisticated network that governs the fate of cancer cells under therapeutic pressure.
Keywords: non-small cell lung cancer, epidermal growth factor receptor, tyrosine kinase inhibitors, drug resistance, microRNA
1Department of Thoracic Oncology, Hangzhou Cancer Hospital, Affiliated Hangzhou First People’s Hospital, Westlake University School of Medicine, Hangzhou, Zhejiang, People’s Republic of China; 2The Fourth School of Clinical Medicine, Zhejiang Chinese Medical University, Hangzhou, Zhejiang, People’s Republic of China
Correspondence: Jie Huang, Email drhunter@aliyun.com
Abstract: Non-small cell lung cancer (NSCLC) harboring activating mutations in the Epidermal Growth Factor Receptor (EGFR) has been effectively treated with EGFR tyrosine kinase inhibitors (TKIs). However, the clinical efficacy of these targeted therapies is invariably limited by the development of acquired resistance. While secondary mutations like T790M and bypass pathway activation are well-documented mechanisms, there is a growing appreciation for the profound role of epigenetic regulators, particularly microRNAs (miRNAs), in orchestrating the resistant phenotype. This review provides a comprehensive and detailed analysis of the multifaceted roles of miRNAs in the emergence and maintenance of EGFR-TKI resistance in NSCLC, including their regulation of alternative receptor tyrosine kinase signaling pathways, driving phenotypic plasticity, specifically the epithelial-mesenchymal transition (EMT) and the acquisition of cancer stem cell (CSC) characteristics, as well as dysregulating core cellular processes, such as apoptosis. We further examine the complex interplay within competing endogenous RNA (ceRNA) networks, where long non-coding RNAs and circular RNAs sequester miRNAs, thereby modulating the expression of resistance-associated genes. Finally, the potential of specific miRNAs as circulating biomarkers for monitoring treatment response and as therapeutic targets to overcome resistance is discussed. This review underscores the central role of miRNA-mediated gene regulation as a critical layer of complexity in EGFR-TKI resistance, highlighting a sophisticated network that governs the fate of cancer cells under therapeutic pressure.
Keywords: non-small cell lung cancer, epidermal growth factor receptor, tyrosine kinase inhibitors, drug resistance, microRNA