Aim: To explore the expression and biological function of long intergenic non-protein coding RNA 1089 (LINC01089) in gastric cancer (GC) progression and its underlying mechanism.
Methods: LINC01089 and microRNA-27a-3p (miR-27a-3p) expressions were detected with the quantitative real-time polymerase chain reaction (RT-qPCR). Cell proliferation, migration and invasion were evaluated by Cell Counting Kit-8 (CCK-8) and Transwell assay. Epithelial–mesenchymal transition (EMT)-related proteins were also measured by Western blot. The relationship between LINC01089 and miR-27a-3p was revealed by a bioinformatics analysis and dual-luciferase reporter assay.
Results: LINC01089 was significantly down-regulated in GC tissues, as well as GC cell lines. GC patients with lower LINC01089 expression were more likely to have poor outcomes. Overexpression of LINC01089 significantly suppressed GC cells growth, migration and invasion and forbade the EMT process. LINC01089 was directly targeted at miR-27a-3p. The transfection of miR-27a-3p mimics reversed the inhibitory effects on proliferative and metastatic abilities of GC cells with LINC01089 overexpression.
Conclusion: LINC01089 inhibits cell proliferation and metastasis in GC by targeting miR-27a-3p/EMT axis, which should be considered as a promising therapeutic target.
Keywords: LINC01089, miRNA-27a-3p, proliferation, metastasis, epithelial-mesenchymal transition (EMT), gastric cancer (GC)