Wu Jingyi, Wu Xiangfei, Wang Jing, Feng Guili, Wang Yuhan, Chen Zide, Wang Wei, Wang Rong
Department of Radiation Oncology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, People's Republic of China.
Department of Neurosurgery, Guangdong Sanjiu Brain Hospital, Guangzhou, Guangdong, People's Republic of China.
Cancer Med. 2025 Apr;14(7):e70827. doi: 10.1002/cam4.70827.
Non-small cell lung cancer patients with EGFR mutation have a high rate of brain metastases, and EGFR tyrosine kinase inhibitors (TKIs) are the principal therapeutic approach. However, acquired targeted therapy resistance is the main reason for EGFR-TKIs' treatment failure. At present, the mechanism of intracranial acquired targeted therapy resistance is limited, mainly due to the lack of a cell line that can be used for its study.
A brain parenchymal metastatic sample that progressed after third-generation EGFR-TKI treatment was used to establish a cell line named AlmoR1. The genetic characteristics of the cell line were evaluated by short tandem repeat (STR) profiling and whole-exome sequencing analysis. The phenotypic characteristics were characterized by CCK8, western blot, HE staining, immunohistochemistry (IHC), and orthotopic brain tumor model.
The cell line we successfully established, AlmoR1, can be passed in vitro stably. STR analysis revealed it was a novel NSCLC BM cell line. It harbors the EGFR E746_A750del (ex19del) mutation, and the IC50 to almonertinib and osimertinib of AlmoR1 was significantly higher than that of sensitive cells. In our orthotopic brain tumor model construction with AlmoR1 cells, 75% (3/4) tumor formation can be observed in the living system.
These data suggest that the established cell line, AlmoR1, preserved the resistance to broad third-generation EGFR-TKIs and good tumorigenicity in an intracranial orthotopic model, so that it can serve as a new tool to elucidate the pathogenesis, explore new treatment methods, and conduct the development of new drugs for targeted therapy resistance of brain metastases.
表皮生长因子受体(EGFR)突变的非小细胞肺癌患者脑转移发生率高,EGFR酪氨酸激酶抑制剂(TKIs)是主要治疗手段。然而,获得性靶向治疗耐药是EGFR-TKIs治疗失败的主要原因。目前,颅内获得性靶向治疗耐药的机制尚不明确,主要是由于缺乏可用于研究的细胞系。
采用经第三代EGFR-TKI治疗后进展的脑实质转移样本建立细胞系,命名为AlmoR1。通过短串联重复序列(STR)分析和全外显子测序分析评估该细胞系的遗传特征。采用CCK8、蛋白质免疫印迹法、苏木精-伊红(HE)染色、免疫组织化学(IHC)及原位脑肿瘤模型等方法对其表型特征进行鉴定。
我们成功建立的细胞系AlmoR1在体外可稳定传代。STR分析显示其为一种新型非小细胞肺癌脑转移细胞系。该细胞系携带EGFR E746_A750del(外显子19缺失)突变,对阿美替尼和奥希替尼的半数抑制浓度(IC50)显著高于敏感细胞。在我们用AlmoR1细胞构建的原位脑肿瘤模型中,在活体系统中可观察到75%(3/4)的肿瘤形成。
这些数据表明,所建立的细胞系AlmoR1在颅内原位模型中保留了对多种第三代EGFR-TKIs的耐药性和良好的致瘤性,可作为阐明发病机制、探索新治疗方法及开展脑转移靶向治疗耐药新药研发的新工具。