RESUMO
Long non-coding RNA LINC01106 is an lncRNA aberrantly expressed in gastric cancer (GC). However, the accurate function remains unclear. The objective of this investigation is to explore detailed regulatory mechanism of lncRNA LINC01106 in GC. The expression of lncRNA LINC01106, MYCN, and miR-34a-5p was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Cell viability was examined using MTT assay. Migratory and invasive abilities of GC cells were evaluated by transwell assay. The targeting relation among lncRNA LINC01106, MYCN, and miR-34a-5p was tested by dual-luciferase reporter (DLR) assay. Relative protein expression of MYCN was assessed via western blot. Besides, a xenograft mouse model was established to assess the role of LINC01106 in GC in vivo. LncRNA LINC01106 and MYCN expression were boosted and miR-34a-5p expression was reduced in GC cells and tissues compared to their controls. Functionally, decreased lncRNA LINC01106 or increased miR-34a-5p restrained GC cells in viability, invasion, and migration in vitro. LINC01106 down-regulation suppressed tumor growth of mice in vivo. In terms of mechanism, lncRNA LINC01106 directly targeted miR-34a-5p and was inversely correlated with miR-34a-5p. MYCN was targeted by miR-34a-5p and was inversely correlated with miR-34a-5p. There was a positive correlation between LINC01106 and MYCN. LINC01106 knockdown led to the suppression of cell invasion, migration, and viability, whereas these effects caused by LINC01106 knockdown were reversed by miR-34a-5p down-regulation or MYCN up-regulation in GC cells. Silencing of lncRNA LINC01106 attenuated cell viability, invasion, and migration by sponging miR-34a-5p to target MYCN in GC.