本研究旨在探讨分岬甘草素（formononetin）对三阴性乳腺癌（TNBC）的影响。从TNBC患者收集了临床样本，并通过Kaplan-Meier方法评估了整体生存率。通过免疫组化、免疫荧光和蛋白质印迹分析确定基因表达情况。通过CCK-8、克隆形成实验和碘化丙啶（PI）染色确定细胞功能。进一步通过异种移植实验验证了分岬甘草素（FM）对TNBC的影响。我们发现FM联合治疗抑制了TNBC的转移，并提高了TNBC患者的总体生存率。此外，FM抑制了TNBC细胞的增殖，诱导了线粒体损伤和细胞凋亡。在TNBC组织和细胞中，FM提高了BTB结构域和CNC同源1（BACH1）的表达。然而，抑制BACH1的shRNA逆转了FM的作用，并促进了TNBC细胞的存活。FM抑制了TNBC的肿瘤生长。综上所述，FM通过BACH1/p53信号通路抑制了TNBC的侵袭性。因此，FM可能是TNBC的一种替代策略。

This study aimed to investigate the effects of formononetin on triple negative breast cancer (TNBC). Clinical samples were collected from patients with TNBC. Overall survival rates were evaluated using the Kaplan-Meier method. Gene expression was determined using immunohistochemistry, immunofluorescence and western blot. Cellular functions were determined using CCK-8, colony formation and propidium iodide (PI) staining. Xenograft assay was performed to further verify the effects of formononetin (FM) on TNBC. We found that FM combined therapy suppressed the metastasis of TNBC and increased the overall survival rates of TNBC patients. Moreover, FM suppressed the proliferation and induced mitochondrial damage and apoptosis of TNBC cells. FM increased the expression of the BTB domain and CNC homolog 1 (BACH1) in TNBC tissues as well as cells. However, BACH1 knockdown antagonized the effects of FM and promoted the survival of TNBC cells. FM suppressed the tumor growth of TNBC. Taken together, FM suppressed the aggressiveness of TNBC via BACH1/p53 signaling. Therefore, FM may be an alternative strategy for TNBC.