Bufalin Induces Apoptosis of MDA-MB-231 Cell Through Activation of JNK/p53 Pathway
Pages 47-53
Jian-Yang Hu, Min-Feng Chen, Xue-Ping Lei, Zhen-Jian Zhuo, Hai-Yan Sun, Zhe-Sheng Chen, Zhi Shi, Dong-Mei Zhang and Wen-Cai Ye

DOI: http://dx.doi.org/10.6000/1929-2279.2015.04.02.1

Published: 07 May 2015

Abstract: Cinobufacini has been widely used at oncology clinics in China to treat many kinds of cancers and bufalin is one active compound of it, but the anti-cancer effect and the underlying mechanisms of bufalin on breast cancer cells are still unclear. Our study demonstrated that bufalin could effectively decrease the viability of MDA-MB-231 cells with IC₅₀ values of 152.2 ± 8.0 nM for 24 h and 22.4 ± 2.3 nM for 48 h, respectively. Further study showed that bufalin could trigger MDA-MB-231 cells to undergo apoptosis with up-regulating protein expression of p-JNK/JNK, p53, p-ERK/ERK, Puma and down-regulating protein expression of Bcl-2, supporting the possible application of bufalin to breast cancer treatment.

Keywords: Apoptosis, JNK, p53, Bcl-2, MDA-MB-231 cell.