Abstract
Long noncoding RNAs (LncRNAs) participate in tumor development and tumorigenesis. However, the mechanism, function and expression of LINC00514 in GC remain unknown. We showed that LINC00514 was upregulated in GC specimens compared with nontumor specimens. Overexpression of LINC00514 induced cell growth and EMT progression in GC cells. By using bioinformatics prediction, we found that miR-204-3p contained binding sequences for LINC00514. Luciferase reporter analysis noted that miR-204-3p overexpression decreased the luciferase expression under LINC00514-wild-type and KRAS-wild-type reporters but not that under mutant reporter. Ectopic LINC00514 expression decreased miR-204-3p expression. miR-204-3p expression was decreased in GC specimens compared with nontumor specimens and that LINC00514 was negatively correlated with miR-204-3p in GC specimens. Furthermore, KRAS was identified as a target gene for miR-204-3p according to TargetScan. Elevated miR-204-3p expression inhibited KRAS expression in HGC-27 cells, and ectopic expression of LINC00514 enhanced KRAS expression. Elevated LINC00514 expression enhanced cell growth and EMT progression by sponging KRAS. Our data indicated that LINC00514 may act as an oncogene and therapeutic target for GC.