乳腺癌是女性癌症相关死亡的主要原因。三阴性乳腺癌 (TNBC) 亚型是最具侵袭性的乳腺癌形式，缺乏生物标志物和有效的靶向治疗。其高度异质性以及先天性和获得性的治疗耐药性为 TNBC 取得积极的临床结果造成了进一步的障碍。因此，开发新的TNBC治疗方法具有很高的临床意义。靶向药物和放射治疗 (RT) 的多模式方法有望提高治疗效果和规避耐药性。在这里，我们使用各种 TNBC 细胞系 MDA-MB-468、MDA-MB-231 和 SUM-159 检查了极光激酶 B (AURKB) 抑制剂 AZD1152 作为单一药物以及与 RT 联合使用的抗癌作用。我们观察到 AZD1152 单独有效抑制 TNBC 细胞系中的集落形成。与单药治疗相比，IC50浓度的AZD1152与电离辐射的组合进一步减少了集落形成。我们的数据支持这样的观点，即抑制 AURKB 通路是治疗 TNBC 和放射增敏的一种有前途的策略，并值得进一步的转化研究。© 2024 Pellizzari 等人。

Breast cancer is a leading cause of cancer-related deaths in females. Triple-negative breast cancer (TNBC) subtype is the most aggressive form of breast cancer that lacks biomarkers and effective targeted therapies. Its high degree of heterogeneity as well as innate and acquired resistance to treatment creates further barriers in achieving positive clinical outcomes in TNBC. Thus, development of novel treatment approaches in TNBC is of high clinical significance. Multimodality approaches with targeted agents and radiotherapy (RT) are promising for increasing efficacy of treatment and circumventing resistance. Here we examined anticancer effects of the Aurora Kinase B (AURKB) inhibitor AZD1152 as a single agent and in combination with RT using various TNBC cell lines, MDA-MB-468, MDA-MB-231 and SUM-159. We observed that AZD1152 alone effectively inhibited colony formation in TNBC cell lines. The combination of AZD1152 at IC50 concentrations together with ionizing radiation further reduced colony formation as compared to the single agent treatment. Our data support the notion that inhibition of the AURKB pathway is a promising strategy for treatment and radiosensitization of TNBC and warrants further translational studies.© 2024 Pellizzari et al.