Emerging studies have indicated that long noncoding RNAs (lncRNAs) possess various functions in initiating human cancers. However, the role of lncRNAs in hepatocellular carcinoma (HCC) still remains ill understood. In this study, we sought to investigate the role of lncRNA CACNA1G-AS1 in HCC progression. Through bioinformatics analysis, we found that CACNA1G-AS1 expression was significantly upregulated in HCC tissues compared with that in the adjacent normal tissues. Moreover, CACNA1G-AS1 upregulation indicated poor prognosis in HCC patients. Knockdown of CACNA1G-AS1 attenuated the proliferation, migration, and invasion of HCC cells. Additionally, decreased expression of CACNA1G-AS1 prevented epithelial-mesenchymal transition. In vivo assay also showed that CACNA1G-AS1 silencing HCC cells have smaller tumor volumes and weights. Further investigations demonstrated that CACNA1G-AS1 worked as a competing endogenous RNA to bind microRNA-2392 (miR-2392) and thereby alleviate the repression of the downstream target C1orf61. Collectively, CACNA1G-AS1 promotes HCC progression through regulating the miR-2392/C1orf61 pathway.
Keywords: C1orf61; CACNA1G-AS1; hepatocellular carcinoma; long noncoding RNA; miR-2392.
© 2019 Wiley Periodicals, Inc.