Dela Cruz Ma Carmela P, Medina Paul Mark B
Biological Models Laboratory, Department of Biochemistry and Molecular Biology, College of Medicine, University of the Philippines Manila, Manila City, Metro Manila 1000, Philippines.
Cancer Pathog Ther. 2024 Jul 6;3(3):215-225. doi: 10.1016/j.cpt.2024.07.001. eCollection 2025 May.
Epithelial-mesenchymal transition (EMT) is a biological process that involves the transformation of epithelial cells into cells with a mesenchymal phenotype, enhancing their migratory and invasive capabilities. EMT is crucial in embryonic development, tissue healing, and wound repair, and aids in forming diverse cell types and structures. However, aberrant EMT is involved in pathogenic processes, including fibrosis, cancer development, and progression. Recent studies show that EMT contributes to resistance to cancer treatment, including epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) therapy in non-small cell lung cancer (NSCLC). This review discusses the intricate relationship between EMT and acquired chemoresistance to EGFR-TKIs. It details evidence on how EGFR-TKIs might induce EMT and how EMT may cause EGFR-TKI resistance. Understanding these pathways is crucial for developing effective prognostic and therapeutic strategies to predict and combat acquired chemoresistance in NSCLC, advancing the field toward more targeted and personalized treatment approaches.
上皮-间质转化（EMT）是一个生物学过程，涉及上皮细胞转变为具有间质表型的细胞，增强其迁移和侵袭能力。EMT在胚胎发育、组织愈合和伤口修复中至关重要，并有助于形成多种细胞类型和结构。然而，异常的EMT参与了包括纤维化、癌症发生和进展在内的致病过程。最近的研究表明，EMT导致对癌症治疗的耐药性，包括非小细胞肺癌（NSCLC）中的表皮生长因子受体-酪氨酸激酶抑制剂（EGFR-TKI）治疗。本综述讨论了EMT与对EGFR-TKIs获得性化疗耐药之间的复杂关系。详细阐述了关于EGFR-TKIs如何诱导EMT以及EMT如何导致EGFR-TKI耐药的证据。了解这些途径对于制定有效的预后和治疗策略以预测和对抗NSCLC中的获得性化疗耐药至关重要，推动该领域朝着更具针对性和个性化的治疗方法发展。
