Overexpression of lncRNA PIK3CD-AS1 promotes expression of LATS1 by competitive binding with microRNA-566 to inhibit the growth, invasion and metastasis of hepatocellular carcinoma cells

Background This study is conducted to investigate the effect of lncRNA PIK3CD-AS1 on the growth and metastasis of hepatocellular carcinoma (HCC) and its potential mechanism. Methods Hepatocellular carcinoma tissues and adjacent normal tissues together with HCC cells and normal liver cells were obtained for detecting expression of PIK3CD-AS1, microRNA-566 (miR-566) and LATS1. Additionally, a series of experiments were performed to determine cell proliferation, migration, invasion, cell cycle distribution and apoptosis of HCC cells. The xenograft tumor model of HCC was established and the growth rate and weight of xenograft tumor in nude mice were compared. Furthermore, the binding site between PIK3CD-AS1 and miR-566 as well as between miR-566 and LATS1 were verified. Results LncRNA PIK3CD-AS1 was downregulated in HCC tissues and cells, and mainly located in cytoplasm. Overexpression of PIK3CD-AS1 inhibited proliferation, colony formation, invasion, migration, epithelial-mesenchymal transition (EMT) and cell cycle progression and promoted apoptosis of HCC cells. Overexpression of PIK3CD-AS1 decreased the growth rate and weight of xenograft tumor in nude mice PIK3CD-AS1 competitively combined with miR-566 to regulate expression of LAST1. Conclusion Collectively, our study suggests that the expression of PIK3CD-AS1 was down-regulated in HCC, and overexpression of PIK3CD-AS1 promoted the expression of LATS1 by competitive binding of miR-566 to inhibit the growth, invasion and metastasis of HCC cells.