Gastric cancer (GC) poses a serious threat to human life, whereas its pathogenesis remains elusive. The present study aimed to investigate the potential pathogenic mechanism behind gastric cancer development. RT-PCR analysis using divergent primers, RNase R digestion assay, and mRNA stability assay were performed to characterize circCOL6A3 (ID: hsa_circ_0006401) in GC cell lines; Western blot was conducted to detect the expression of COL6A3. Cell counting kit-8 (CCK-8), EdU incorporation assay, and Transwell were run to evaluate GC cell proliferation and migration. Luciferase reporter assay was performed to validate the relationship between miR-3064-5p and COL6A3. Both circCOL6A3 and COL6A3 were highly expressed in GC cells, while miR-3064-5p was down-regulated. Depleted circCOL6A3 significantly decreased cell viability and mobility, and increased cell apoptosis. CircCOL6A3 regulated the expression of miR-3064-5p, and the effect of si-circCOL6A3 on cell biological behaviors was abolished by miR-3064-5p inhibitor. MicroRNA-3064-5p targets COL6A3 to regulate its expression. Taken together, the present study indicated that overexpressed circCOL6A3 promoted cell proliferation, migration and apoptosis of gastric cancer through rescission of miR-3064-5p-induced inhibitory effect on COL6A3. Our study will furnish theoretical grounds for future clinical diagnosis and treatment of GC patients.
Keywords: COL6A3; Gastric cancer; Proliferation and migration; circCOL6A3; microRNA-3064–5p.
Copyright © 2019 Elsevier Inc. All rights reserved.