Licochalcone A Inhibits the Proliferation of Human Lung Cancer Cell Lines A549 and H460 by Inducing G2/M Cell Cycle Arrest and ER Stress.
Licochalcone A Inhibits the Proliferation of Human Lung Cancer Cell Lines A549 and H460 by Inducing G2/M Cell Cycle Arrest and ER Stress.
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甘草查耳酮 A 通过诱导 G2/M 细胞周期停滞和 ER 应激抑制人肺癌细胞系 A549 和 H460 的增殖
DOI：
10.3390/ijms18081761
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发表时间：
2017-08-12
影响因子：
5.6
通讯作者：
Liang G
中科院分区：
文献类型：
--
作者：
Qiu C;Zhang T;Zhang W;Zhou L;Yu B;Wang W;Yang Z;Liu Z;Zou P;Liang G
甘草酮A(LICA)是从著名中草药甘草中分离得到的一种黄酮类化合物，具有广泛的药理活性。本研究探讨了LICA对非小细胞肺癌(NSCLC)细胞的抗癌作用及其可能机制。LICA以剂量依赖的方式降低NSCLC细胞的存活率并诱导其凋亡。LICA通过阻断G2/M期细胞周期进程和诱导细胞凋亡来抑制肺癌细胞的生长。LICA作用于H460和A549癌细胞后，MDM2、Cyclin B1、CDc2和CDc25C的表达均下降。此外，LICA还诱导了caspase-3的激活和多聚ADP核糖聚合酶(PARP)的裂解，呈现出凋亡信号的特征。此外，LICA还增加了内质网应激相关蛋白的表达，如p-eIF2α和ATF4。这些数据提供了LICA有潜力用于肺癌治疗的证据。
Licochalcone A (LicA), a flavonoid isolated from the famous Chinese medicinal herb Glycyrrhiza uralensis Fisch, has wide spectrum of pharmacological activities. In this study, the anti-cancer effects and potential mechanisms of LicA in non-small cell lung cancer (NSCLC) cells were studied. LicA decreased cell viability and induced apoptosis in a dose-dependent manner in NSCLC cells. LicA inhibited lung cancer cells growth by blocking cell cycle progression at the G2/M transition and inducing apoptosis. LicA treatment decreased the expression of MDM2, Cyclin B1, Cdc2 and Cdc25C in H460 and A549 cancer cell lines. In addition, LicA induced caspase-3 activation and poly-ADP-ribose polymerase (PARP) cleavage, which displayed features of apoptotic signals. Furthermore, LicA increased the expression of endoplasmic reticulum (ER) stress related proteins, such as p-EIF2α and ATF4. These data provide evidence that LicA has the potential to be used in the treatment of lung cancer.
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