LAUSR

Overexpression of long noncoding RNA (lncRNA) H19 has been observed in various cancers, which indicates that H19 exert important roles in the progression of carcinogenesis. MiR‐326 has been reported to play tumor suppressive roles in multiple tumors. Recently, the competing endogenous RNA (ceRNA) hypothesis has implied that lncRNAs might function as molecular sponges for microRNAs in various cancers. However, the roles of H19/miR‐326 in human hepatocellular carcinoma (HCC) still remain unclear. The aim of our study was to determine H19/miR‐326 expression in HCC cells and investigate their roles in HCC development. We found that H19 was significantly elevated and miR‐326 was decreased in HCC cells including Hep3B, HepG2, MHCC‐97L, SK‐hep1, Hun7, SMCC‐7721 compared with LO2 cells, respectively. In the subsequent experiments, we observed that inhibition of H19 can repress HCC cell growth, migration, and invasion in vitro. H19 downregulation can increase miR‐326 expression in HCC cells. Meanwhile, miR‐326 mimics can also inhibit HCC progression, whereas miR‐326 inhibitors exhibited a reverse phenomenon by modulating H19 expression. In addition, a negative association between H19 and miR‐326 was predicted and confirmed. Furthermore, the transcription factor TWIST1 has been recognized as a significant regulator in tumor progression. Here, by performing bioinformatics analysis, TWIST1 was identified as a downstream target of miR‐326. The findings of our study implied that lncRNA H19 can serve as a ceRNA to sponge miR‐326 and modulate TWIST1 levels in HCC pathogenesis. Taken these together, these findings indicated that H19/miR‐326/TWIST1 axis was involved in HCC development and can indicate a novel HCC target.