Saikosaponin-d suppresses cell growth in renal cell carcinoma through EGFR/p38 signaling pathway
Saikosaponin-d suppresses cell growth in renal cell carcinoma through EGFR/p38 signaling pathway
复制标题
柴胡皂苷-d 通过 EGFR/p38 信号通路抑制肾细胞癌细胞生长
DOI：
10.4149/neo_2017_405
复制
发表时间：
2017-01-01
期刊：
影响因子：
3
通讯作者：
Dang, Q.
中科院分区：
文献类型：
--
作者：
Cai, C.;Zhang, H.;Dang, Q.
本研究旨在探讨柴胡皂苷d（Saikosaponin-d，SSd）对肾癌细胞生长抑制、诱导凋亡和细胞周期阻滞的作用及其机制。MTT法和集落形成实验结果表明，不同剂量的SSd对肾癌细胞增殖均有抑制作用。流式细胞仪分析显示，SSd通过上调p53蛋白表达，诱导肾癌细胞凋亡，使细胞周期阻滞于G 0/G1期，从而达到抑制肾癌细胞增殖的作用。与对照组相比，SSd能显著抑制769-P和786-O细胞的生长，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诱导肾癌细胞凋亡、抑制细胞生长、上调p53表达等生物学效应的分子基础。总之，我们的数据表明，SSd可以作为一个有前途的干预与RCC患者的化学预防或化疗治疗。
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.