ZNF655 mediated by LINC01210/miR‐124‐3p axis promotes the progression of gastric cancer

Abstract

Abstract Gastric cancer (GC) is a common malignant tumor that usually originates from the epithelium of the gastric mucosa. ZNF655 was a suppressor gene of many cancers. However, the mechanism of ZNF655 in GC remains unknown. Quantitative polymerase chain reaction was used to assess the expression of ZNF655, LINC01210, and miR‐124‐3p. Western blotting was used to monitor ZNF655 protein expression. MTT, clone formation, transwell, and flow cytometry were all used to investigate the functions of GC cells. The interactions between ZNF655, LINC01210, and miR‐124‐3p were confirmed using the dual‐luciferase reporter gene assay and the RIP assay. ZNF655 was highly expressed in GC cells. ZNF655 knockdown reduced GC cell viability, proliferation, migration, invasion, and induced apoptosis. The level of miR‐124‐3p was significantly reduced in GC cells. Besides, miR‐124‐3p targeted ZNF655 and inhibited its expression. MiR‐124‐3p mimics inhibited GC cell progression, but ZNF655 overexpression reversed these effects. Moreover, LINC01210 was found to be highly expressed in GC cells and to be able to sponge miR‐124‐3p. Furthermore, inhibiting miR‐124‐3p or increasing ZNF655 could counteract the effects of LINC01210 knockdown on GC cell development. Finally, ZNF655 promoted GC cell progression and was regulated by the LINC01210/miR‐124‐3p axis.

Keywords

• GC
• LINC01210
• miR‐124‐3p
• ZNF655