LAUSR

OBJECTIVE To clarify the role of lncRNA FOX4-AS1 in the progression of gastric cancer (GC) via interacting with EZH2/LSD1. PATIENTS AND METHODS Relative level of FOXP4-AS1 in GC tissues and adjacent normal tissues was determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The potential influences of FOXP4-AS1 on cellular behaviors of GC cells were evaluated via a series of functional experiments. Bioinformatics prediction, RNA immunoprecipitation (RIP) assay, and Western blot were conducted to verify the potential of EZH2/LSD1 as a target of FOXP4-AS1. RESULTS FOXP4-AS1 was upregulated in GC tissues relative to controls. Its level was higher in GC patients with stage III-IV than those with stage I-II. The survival rate was lower in GC patients presenting the high expression of FOXP4-AS1 compared with those presenting low expression. Transfection of sh-FOXP4-AS1 1# or sh-FOXP4-AS1 2# attenuated proliferative, migratory, and invasive abilities of AGS and BGC7901 cells. FOXP4-AS1 could bind to LSD1 and EZH2, and positively regulated their expression levels. Transfection of sh-LSD1 or sh-EZH2 reduced the proliferative ability of GC cells. CONCLUSIONS FOXP4-AS1 binds to EZH2/LSD1 to form a carcinogenic complex, thus accelerating GC cells to proliferate, migrate and invade.