miR-4513 promotes gastric cancer cell proliferation and epithelial-mesenchymal transition through targeting KAT6B.

Abstract

The purpose of this study was to investigate the expression level of microRNA-4513 (miR-4513) in gastric cancer, and the underlying mechanisms of miR-4513 in regulating gastric cancer (GC) progression. Quantitative real time-polymerase chain reaction (qRT-PCR) was performed to measure the expression level of miR-4513 in GC cells. Transfection efficacy of synthetic miRNAs was examined by qRT-PCR. After synthetic miRNAs transfection, cell counting kit-8 assay and transwell invasion assay was conducted to measure biological changes in these groups. Key molecular expression level involved in epithelial-mesenchymal transition (EMT) was analyzed by western blot. Bioinformatic analysis and western blot were performed to investigate the connection between miR-4513 and lysine acetyltransferase 6B (KAT6B). qRT-PCR results showed miR-4513 expression level was upregulated in GC cell lines. Downregulate miR-4513 expression inhibited GC cell proliferation, invasion, and EMT. KAT6B was validated as a direct target of miR-4513. In addition, KAT6B expression level can be upregulated by miR-4513 inhibitor. Collectively, we showed miR-4513 involved in regulating the biological function of GC cells via KAT6B. In addition, miR-4513 may serve as a potential target for the molecular therapy of GC.