Astragaloside IV inhibits cell migration and viability of hepatocellular carcinoma cells via suppressing long noncoding RNA ATB
Astragaloside IV inhibits cell migration and viability of hepatocellular carcinoma cells via suppressing long noncoding RNA ATB
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DOI：
10.1016/j.biopha.2017.12.108
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发表时间：
2018-03-01
影响因子：
7.5
通讯作者：
Chen, Hongyan
中科院分区：
文献类型：
--
作者：
Li, Yaling;Ye, Yun;Chen, Hongyan
黄芪甲苷（AS-IV）是黄芪的主要活性成分，在某些癌症中显示出有吸引力的抗癌作用。然而，AS-IV在肝细胞癌（HCC）中的作用和作用机制在很大程度上还不清楚。最近发现长链非编码RNA（lncRNA）在HCC的发生和发展中具有重要作用，但lncRNA是否参与AS-IV的抗癌作用尚不清楚。在这项研究中，我们证明，AS-IV显着下调lncRNA-ATB表达的剂量和时间依赖性的方式在肝癌细胞。AS-IV通过下调lncRNA-ATB抑制肝癌细胞的上皮间质转化（EMT）和迁移。此外，通过下调lncRNA-ATB，AS-IV灭活IL-11/STAT 3信号转导，诱导HCC细胞凋亡，并降低HCC细胞活力。lncRNA-ATB的过表达逆转了AS-IV对HCC细胞迁移、EMT、细胞凋亡、细胞活力和IL-11/STAT 3信号转导的影响。综上所述，我们的结果表明，AS-IV通过下调lncRNA-ATB抑制HCC细胞的迁移和细胞活力。因此，我们的数据提供了一个新的分子基础，应用AS-IV治疗肝癌。
Astragaloside IV (AS-IV), the major active component of Astragalus membranaceus, has shown attractive anticancer effects in certain cancers. However, the roles and action mechanisms of AS-IV in hepatocellular carcinoma (HCC) are largely unclear. Long noncoding RNAs (lncRNAs) are recently revealed to have crucial roles in HCC initiation and progression, but whether lncRNAs participate in the anticancer roles of AS-IV are unknown. In this study, we demonstrated that AS-IV significantly downregulated lncRNA-ATB expression in a dose-and time-dependent manner in HCC cells. Through downregulating lncRNA-ATB, AS-IV repressed epithelial-mesenchymal transition (EMT) and migration of HCC cells. Furthermore, through downregulating lncRNA-ATB, AS-IV inactivated IL-11/STAT3 signaling, induced HCC cell apoptosis, and decreased HCC cell viability. Overexpression of lncRNA-ATB reversed the effects of AS-IV on HCC cell migration, EMT, cell apoptosis, cell viability, and IL-11/STAT3 signaling. Taken together, our results showed that AS-IV inhibited migration and cell viability of HCC cells via downregulating lncRNA-ATB. Thus, our data provided a novel molecular basis for the applications of AS-IV in the therapy of HCC.