Abstract
Gastric cancer (GC) still poses a significant threat to human life. Hence, there is an urgent need to understand the mechanism of GC progression and develop novel therapeutics approach to treating GC. This study was conducted to evaluate the role of the lncRNA SNHG22 in the progression of GC. First, GC data from TCGA were analyzed using GEPIA. After the starbase database was used to predict SNHG22 target miRNA and miR-101-3p target mRNA. The predictions were validated using a dual-luciferase reporter assay, biotinylated RNA pull-down assay, and RIP-qRT-PCR. The relative expression of SNHG22, miR-101-3p, and E2F2 was measured by qRT-PCR and western blot (WB) analysis, while the mechanism of GC cell proliferation was elucidated through the colony formation and CCK-8 assay. Our result showed that SNHG22 was upregulated significantly in GC tissue samples from TCGA database, GC cell lines, and clinical tissue samples, and its expression was related to low survival rate of gastric cancer patients. Bioinformatics prediction predicted miR-101-3p as the potential target of SNHG22 and E2F2 genes as miR-101-3p target mRNA. We found that E2F2 expression was negatively associated with overall survival of GC patients. Functional study showed that silencing SNHG22 markedly inhibited the proliferation, migration, and invasion of GC cells as well as in vivo tumor growth. This was reversed after inhibiting miR-101-3p or overexpressing E2F2. The lncRNA SNHG22 promotes the proliferation, migration, and invasion of GC cells via the miR-101-3p/E2F2 axis. SNHG22 might be a potential prognostic indicator in gastric cancer.