Home Neoplasma 2017 Neoplasma Vol.64, No.4, p.518-525, 2017

Journal info

6 times a year.
Founded: 1954
ISSN 0028-2685
ISSN 1338-4317 (online)

Published in English

Editorial Info
Abstracted and Indexed
Submission Guidelines

Select Journal

Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Neoplasma Vol.64, No.4, p.518-525, 2017

Title: Saikosaponin-d suppresses cell growth in renal cell carcinoma through EGFR/p38 signaling pathway
Author: C. Cai, H. Zhang, Y. Ou, Y. Jiang, D. Zhong, H. Qi, Q. Dang

Abstract: 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.

Keywords: Saikosaponin-d, RCC, cell growth, EGFR/p38
Published online: 11-Jul-2017
Year: 2017, Volume: 64, Issue: 4 Page From: 518, Page To: 525

download file

© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.