Yang Lichang, Chang Ru, Pan Jianzhen, Huang Shan
Anhui University of Chinese Medicine, Hefei, 230012, China.
Nanjing University of Chinese Medicine, Nanjing, 210023, Jiangsu, China.
Hereditas. 2025 Jul 24;162(1):140. doi: 10.1186/s41065-025-00510-8.
Saikosaponin D (SSD) has been shown to have the strongest anti-tumor activity. This study aimed to explore the effects and potential molecular mechanism of Saikosaponin D (SSD) against estrogen receptor-positive breast cancer.
MCF-7 and T-47D cell lines were treated with a series of concentrations of SSD. Growth, cell cycle distribution, and apoptosis tests were performed. Next, potential targets of SSD against breast cancer were predicted. The targets for SSD were collected from HERB database and PharmMapper Server and displayed accoding to degree.
there was a dose-dependent decrease in MCF-7 and T-47D cancer cell viability and the the half maximal inhibitory concentrations were 7.31 ± 0.63 µM and 9.06 ± 0.45 µM, respectively. Treatment with SSD decreased cell proliferation, arrested cell cycle at G1, and induced cell apoptosis. There were 227 potential targets of SSD against breast cancer, among which ESR1 was a hub gene. SSD treatment can reduce the protein levels of estrogen receptor α (ERα), Cyclin D1 (CCND1), and the proto-oncogene c-Myc (c-Myc).
SSD may have therapeutic potential in estrogen receptor-positive breast cancer, may through its suppression on ESR1.
柴胡皂苷D（SSD）已被证明具有最强的抗肿瘤活性。本研究旨在探讨柴胡皂苷D（SSD）对雌激素受体阳性乳腺癌的作用及潜在分子机制。
用一系列浓度的SSD处理MCF-7和T-47D细胞系。进行生长、细胞周期分布和凋亡检测。接下来，预测SSD抗乳腺癌的潜在靶点。从HERB数据库和PharmMapper服务器收集SSD的靶点，并按程度显示。
MCF-7和T-47D癌细胞活力呈剂量依赖性下降，半数最大抑制浓度分别为7.31±0.63μM和9.06±0.45μM。SSD处理可降低细胞增殖，使细胞周期停滞在G1期，并诱导细胞凋亡。SSD抗乳腺癌的潜在靶点有227个，其中ESR1是一个枢纽基因。SSD处理可降低雌激素受体α（ERα）、细胞周期蛋白D1（CCND1）和原癌基因c-Myc（c-Myc）的蛋白水平。
SSD在雌激素受体阳性乳腺癌中可能具有治疗潜力，可能是通过其对ESR1的抑制作用。
