Long noncoding RNA BLACAT1 is overexpressed in hepatocellular carcinoma and its downregulation suppressed cancer cell development through endogenously competing against hsa-miR-485-5p

Abstract

ObjectiveIn this work, we explored the expression and mechanistic role of long noncoding RNA (lncRNA), bladder cancer associated transcript 1 (BLACAT1) in human hepatocellular carcinoma (HCC). MethodsBLACAT1 expression in bothin vitro HCC cell lines and in vivo human HCC clinical samples were assessed by qRT-PCR. In HeG2 and MHCC97 L cells, BLACAT1 downregulation was induced by lentiviral infection to evaluate its functions in regulating HCC cancer cell proliferation and invasion in vitro, and xenograft in vivo. A BLACAT1 endogenously competing candidate, human microRNA-485-5p (has-miR-485-5p) was assessed in dual-luciferase assay and qRT-PCR in HCC cells. Furthermore, has-miR-485-5p was inhibited in BLACAT1-downregulated HeG2 and MHCC97 L cells to evaluate the correlation of has-miR-485-5p in BLACAT1-associated functional regulation in HCC cells. ResultsBLACAT1was found to be overexpressed in both HCC cells and human HCC tumors. In HeG2 and MHCC97 L cells, lentivirus-induced BLACAT1 downregulation inhibited cancer cellin vitro proliferation and invasion, and in vivo xenograft growth. Has-miR-485-5p was confirmed to be bound by BLACAT1 and its expression in HCC cells inversely regulated by BLACAT1. Then, has-miR-485-5p downregulation reversed the inhibitory effects of BLACAT1 downregulation on HCC cancer cell in vitro functions. ConclusionBLACAT1 is aberrantly upregulated in HCC and its inhibition had tumor suppressing effects in human HCC, possibly through endogenously competing against has-miR-485-5p. The BLACAT1/ has-miR-485-5p regulatory axis may be a molecular target for future HCC therapy.