LAUSR

Antisense non-coding RNA in the INK4A locus (ANRIL) has been recognized as a cancer-related lncRNA in hepatocellular carcinoma previously. This study aimed to reveal the functional effects and mechanisms of ANRIL on hepatocellular carcinoma cells in vitro. The expression of ANRIL in hepatocellular carcinoma cell lines (MHCC97 and Li-7) and non-tumourigenic liver cell line THLE-3 was detected by qRT-PCR. The expression of ANRIL, miR-144 and PBX3 in hepatocellular carcinoma cells was altered simultaneously or respectively by vector/oligonucleotide transfection. Then, cell viability, migration, invasion, apoptotic cell rate, protein expression of apoptosis-related factors were assessed. The correlation between ANRIL, miR-144 and PBX3 was explored. ANRIL was highly expressed in MHCC97 and Li-7 cells when compared to THLE-3 cells. ANRIL overexpression promoted cell viability, migration, invasion and suppressed apoptosis of MHCC97 and Li-7 cells. ANRIL negatively regulated miR-144, and oncogenic effects of ANRIL were attenuated when miR-144 was overexpressed. PBX3 was a direct target of miR-144. miR-144 overexpression blocked PI3K/AKT and JAK/STAT signalling pathways via targeting PBX3. Our data documented that ANRIL promoted hepatocellular carcinoma cells growth, migration and invasion. One of the possible mechanisms responsible for the tumour-promoting actions is that ANRIL sponging miR-144 to derepress PBX3.