Ziyuglycoside II inhibits the growth of human breast carcinoma MDA-MB-435 cells via cell cycle arrest and induction of apoptosis through the mitochondria dependent pathway

24Citations
Citations of this article
11Readers
Mendeley users who have this article in their library.

Abstract

Ziyuglycoside II is one of the major active compounds of Sanguisorba officinalis L., which has a wide range of clinical applications including hemostasis, antibiosis, anti-inflammation and anti-oxidation. This study investigated the effect of ziyuglycoside II on the growth of human breast carcinoma MDA-MB-435 cells for the first time. The results showed that ziyuglycoside II could significantly inhibit the growth of MDA-MB-435 cells through blocking cell cycle progression at G0/G1 and S phase as well as via inducing cell apoptosis. Accumulation of reactive oxygen species (ROS) was observed in the progression of cell cycle arrest, which was associated with the increased expression of cell cycle regulating factors, p53 and p21. Subsequent apoptosis induced by ziyuglycoside II was accompanied with the activation of mitochondrial pathway, in particular a decreased mitochondrial membrane potential (MMP) as well as increased Bax/Bcl-2 ratio, cytochrome c release and the activity of caspase-3 and caspase-9. In conclusion, our study was the first to report that ziyuglycoside II has inhibitory effect on the growth of MDA-MB-435 cells, which might become a potential therapeutic approach of breast cancer in the future. © 2013 by the authors; licensee MDPI, Basel, Switzerland.

Cite

CITATION STYLE

APA

Zhu, X., Wang, K., Zhang, K., Huang, B., Zhang, J., Zhang, Y., … Zhou, F. (2013). Ziyuglycoside II inhibits the growth of human breast carcinoma MDA-MB-435 cells via cell cycle arrest and induction of apoptosis through the mitochondria dependent pathway. International Journal of Molecular Sciences, 14(9), 18041–18055. https://doi.org/10.3390/ijms140918041

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free