Inhibition of AKT/FoxO3a signaling induced PUMA expression in response to p53-independent cytotoxic effects of H1: A derivative of tetrandrine
作者： Yin-Xu Zhang , Xiao-Mei Liu , Jing Wang , Jun Li , Ying Liu
DOI: 10.1080/15384047.2015.1040950
关键词:
摘要: PUMA (p53 unregulated modulator of apoptosis), a BH3-only Bcl-2 family member, can be induced by p53-dependent and p53-independent manners. It plays an important role as regulator cellular apoptosis. Herein, we evaluate the effects H1 (a derivative tetrandrine) on induction underlie its potential mechanism in cytotoxic response. Anti-proliferative activity evidently were observed wild-type p53 null cells. Further studies demonstrated that resulted increase cleaved PARP, decease survivin elevation p-H2AX. What is more, significantly expression concentration- time-dependent manner caused Bax/Bcl-2 ratio Of note, knockdown attenuated H1. inhibition AKT/FoxO3a signaling contributed to H1-mediated induction. Targeted suppression siRNA could overcome In addition, suppressed NF-κB early apoptotic late cells, elevated caspase-3 activity. Taken together, found may contribute induction, suggesting result response
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