Long non-coding RNA XIST accelerates hepatic carcinoma progression by targeting the microRNA-320a/PIK3CA axis

The aim of the present study was to reveal the new molecular mechanism of long non-coding (lnc)RNA XIST in the development of hepatic carcinoma. A total of 69 patients with hepatic carcinoma were included. Hepatoma cell lines (SUN449), hepatoblastoma cell line (HepG2, Huh-6), liver cancer cell line (HepG2) and transformed human liver epithelial-2 cells (THLE-2) were used in the present study. A total 3 short hairpin RNA (sh)-lncRNA XIST sequences, overexpression vector (oe)-lncRNA XIST, microRNA (miR)-320a mimic, miR-320a inhibitor, PIK3CA inhibitor, and their corresponding controls were transfected in hepatic carcinoma cells. Reverse transcription-quantitative polymerase chain reaction was conducted to detect lncRNA-XIST, miR-320a and PIK3CA expression. Cell Counting Kit-8 assay and flow cytometry were undertaken to measure proliferation and apoptosis. Cell invasion and migration were detected by Transwell assays. Moreover, the binding of lncRNA XIST, PIK3CA and miR-320a were verified by luciferase reporter experiment and pull-down assay. Finally, a rescue assay was processed to confirm the effect of lncRNA-XIST, miR-320a and PIK3CA in the aforementioned processes. lncRNA XIST was highly expressed in hepatic carcinoma tissues and cells. The survival rate was significantly lower in the highly expressed lncRNA XIST group. shlncRNA XIST attenuated cell proliferation, invasion and migration, while increasing the apoptosis of hepatic carcinoma cells. The lncRNA XIST negatively targeted miR-320a, and miR-320a negatively regulated the expression of PIK3CA. The miR-320a mimic and PIK3CA inhibitor could recover the effect of oe-lncRNA in terms of the proliferation, invasion, migration and apoptosis of hepatic carcinoma cells. lncRNA XIST accelerates hepatic carcinoma progression by targeting the miR-320a/PIK3CA axis, which might provide the theoretical basis for the potential targeted therapy of hepatic carcinomas.