lncRNA LIFR‑AS1 inhibits gastric carcinoma cell proliferation, migration and invasion by sponging miR‑4698.

The vital functions of long non‑coding (lnc)RNAs have been verified in gastric carcinoma (GC). However, as a novel cancer‑related lncRNA, the influence of leukemia inhibitory factor receptor antisense RNA 1 (LIFR‑AS1) in GC cell biological behaviors remains unreported. The present study explored the biological effects of lncRNA LIFR‑AS1 on GC progression. Reverse transcription‑quantitative PCR was performed to examine lncRNA LIFR‑AS1 expression in GC tissues and cells. Cell Counting Kit‑8, 5‑ethynyl‑2'‑deoxyuridine incorporation, cell wound healing and Transwell invasion assays were used to assess the functions of lncRNA LIFR‑AS1 in GC cell proliferation, migration and invasion. Additionally, associations among lncRNA LIFR‑AS1, microRNA (miR)‑4698 and microtubule‑associated tumor suppressor 1 (MTUS1) were investigated via bioinformatics software and a luciferase reporter system. In addition, western blotting was used to examine the expression of MEK and ERK. Decreased lncRNA LIFR‑AS1 expression was observed in GC tissues and cells. Upregulated lncRNA LIFR‑AS1 inhibited GC cell proliferation, migration and invasion. Upregulated miR‑4698 and downregulated MTUS1 were identified in GC tissues and cells. The inhibitory interaction between lncRNA LIFR‑AS1 and miR‑4698 was confirmed. Additionally, MTUS1 was predicted as a target gene of miR‑4698 positively regulated by lncRNA LIFR‑AS1. The MEK/ERK pathway was inhibited by lncRNA LIFR‑AS1 via regulating MTUS1. These findings revealed the inhibitory functions of lncRNA LIFR‑AS1 in GC cell proliferation, migration and invasion. The process was mediated via miR‑4698, MTUS1 and the MEK/ERK pathway.