Neoplasma. 2017;64(4):518-525. doi: 10.4149/neo_2017_405.
The study aimed to explore the effect of Saikosaponin-d (SSd) and its underlying mechanism on cell growth inhibition as well as induction of apoptosis and cell cycle arrest in renal cell carcinoma (RCC). MTT assay and colony formation assay were employed in this study, with the results indicating that RCC cells proliferation was inhibited by SSd at different doses. Analysis by flow cytometry revealed that RCC cell proliferation inhibitory effect of SSd was achieved by inducing apoptosis and cell cycle arrest at G0/G1 phase via up-regulation of p53. As compared to the control group, SSd can significantly inhibit the growth of 769-P and 786-O cell lines and induce apoptosis and cell cycle arrest. The mechanism exploration demonstrated that inhibiting the activation of EGFR/p38 signaling pathways was the molecular basis of SSd's biological effects such as inducing apoptotic death, inhibiting cell growth as well as up-regulating p53 expression in human RCC cells. In conclusion, our data suggest that SSd may serve as a promising intervention for chemopreventive or chemotherapeutic treatment for patients with RCC.
本研究旨在探讨柴胡皂苷 d（SSd）对肾细胞癌（RCC）细胞生长抑制、诱导细胞凋亡和细胞周期阻滞的作用及其机制。本研究采用 MTT 法和集落形成实验，结果表明 SSd 以不同剂量抑制 RCC 细胞增殖。通过流式细胞术分析发现，SSd 通过上调 p53 诱导细胞凋亡和 G0/G1 期细胞周期阻滞，从而抑制 RCC 细胞的增殖。与对照组相比，SSd 可显著抑制 769-P 和 786-O 细胞系的生长，并诱导细胞凋亡和细胞周期阻滞。机制探讨表明，抑制 EGFR/p38 信号通路的激活是 SSd 诱导细胞凋亡、抑制细胞生长以及上调人 RCC 细胞中 p53 表达等生物学效应的分子基础。综上所述，本研究结果表明，SSd 可能成为 RCC 患者化学预防或化疗治疗的一种有前途的干预措施。
