Licochalcone B inhibits growth of bladder cancer cells by arresting cell cycle progression and inducing apoptosis
Licochalcone B inhibits growth of bladder cancer cells by arresting cell cycle progression and inducing apoptosis
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甘草查耳酮 B 通过阻止细胞周期进程和诱导细胞凋亡来抑制膀胱癌细胞的生长
DOI：
10.1016/j.fct.2013.12.030
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发表时间：
2014-03-01
影响因子：
4.3
通讯作者：
Wang, Zhiping
中科院分区：
文献类型：
--
作者：
Yuan, Xuan;Li, Tao;Wang, Zhiping
研究甘草查耳酮B（LCB）体外抑制人恶性膀胱癌细胞系（T24和EJ）增殖的机制以及在M849（小鼠膀胱癌细胞系）肿瘤模型中的体内抗肿瘤活性。T24或EJ细胞暴露于LCB以浓度依赖性和时间依赖性方式显著抑制细胞系增殖，并分别导致T24或EJ细胞的S期阻滞。LCB处理降低细胞周期蛋白A、细胞周期蛋白依赖性激酶（CDK 1和CDK 2）mRNA、细胞分裂周期25（Cdc 25 A和Cdc 25 B）蛋白的表达。此外，LCB处理下调Bcl-2和Survivin的表达，增强Bax的表达，激活caspase-3和裂解的聚（ADP-核糖）聚合酶（PARP）蛋白。体外殖民地形成实验和C57 BL/6小鼠体内MB 49肿瘤模型显示，LCB处理的MB 49细胞致瘤性明显降低。这些发现为LCB在化学预防和膀胱癌治疗中的应用提供了支持。(C)2013爱思唯尔有限公司保留所有权利。
To examine the mechanisms by which licochalcone B (LCB) inhibits the proliferation of human malignant bladder cancer cell lines (T24 and EJ) in vitro and antitumor activity in vivo in M849 (murine bladder cancer cell line) tumor model. Exposure of T24 or EJ cells to LCB significantly inhibited cell lines proliferation in a concentration-dependent and time-dependent manner, and resulted in S phase arrest in T24 or EJ cells, respectively. LCB treatment decreased the expression of cyclin A, cyclin-dependent kinase (CDK1 and CDK2) mRNA, cell division cycle 25 (Cdc25A and Cdc25B) protein. In addition, LCB treatment down-regulated Bcl-2 and survivin expression, enhanced Bax expression, activated caspase-3 and cleaved poly (ADP-ribose) polymerase (PARP) protein. Consistently, the tumorigenicity of LCB-treated MB49 cells was limited significantly by using the colony formation assay in vitro and the MB49 tumor model performed in C57BL/6 mice in vivo. These findings provide support for the use of LCB in chemoprevention and bladder cancer therapy. (C) 2013 Elsevier Ltd. All rights reserved.