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

Abstract

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.