Astragaloside IV inhibits cell migration and viability of hepatocellular carcinoma cells via suppressing long noncoding RNA ATB.

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.