Tetrandrine induces apoptosis in human neuroblastoma through regulating the Hippo/YAP signaling pathway

被引:21
|
作者
Zhao, Qian [1 ]
Jia, Xi [2 ]
Zhang, Yuanyuan [3 ]
Dong, Yiping [4 ]
Lei, Yutiantian [4 ]
Tan, Xinyue [4 ]
Williamson, Ramone A. [5 ]
Wang, Aiying [5 ]
Zhang, Dan [5 ]
Ma, Jinlu [4 ]
机构
[1] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Otolaryngol, 277 Yanta West Rd, Xian 710061, Shaanxi, Peoples R China
[2] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Nucl Med, 277 Yanta West Rd, Xian 710061, Shaanxi, Peoples R China
[3] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Pediat, 277 Yanta West Rd, Xian 710061, Shaanxi, Peoples R China
[4] Xi An Jiao Tong Univ, Affiliated Hosp 1, Dept Oncol, 277 Yanta West Rd, Xian 710061, Shaanxi, Peoples R China
[5] Xi An Jiao Tong Univ, Hlth Sci Ctr, Dept Cell Biol & Genet, 76 Yanta West Rd, Xian 710061, Shaanxi, Peoples R China
基金
中国博士后科学基金;
关键词
Neuroblastoma (NB); Tetrandrine (TET); Apoptosis; Hippo/YAP signaling pathway; PROLIFERATION; CELLS; REGENERATION;
D O I
10.1016/j.bbrc.2019.04.075
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Tetrandrine (TET), a bis-benzylisoquinoline alkaloid, shows cytotoxicity against several different types of tumors. However, the mechanism by which TET exerts its anti-cancer capabilities remains unclear. In this study, we confirmed that TET inhibits proliferation and induces apoptosis in neuroblastoma (NB) in vitro and in vivo. Moreover, we revealed that the anti-cancer ability of TET is associated with a decreased expression of anti-apoptotic Bcl-2. Importantly, we demonstrated that the Hippo/YAP pathway is involved in down-regulating of Bcl-2. Notably, YAP overexpression promoted proliferation and suppressed apoptosis, even partially reversed TET-induced effects in NB cells. Our findings support the prospect that TET could be a potential therapeutic agent for NB, and suggest that targeting the Hippo/YAP pathway may represent a valuable approach to NB treatment. (C) 2019 The Authors. Published by Elsevier Inc.
引用
收藏
页码:846 / 851
页数:6
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