miR-384 targeting CTNNB1 regulates EMT and inhibits proliferation in gastric cancer

Abstract Background: MicroRNAs are important for gastric cancer (GC) EMT. This work focused on investigating how miR-384 affected GC and elucidating underlying mechanisms involved. Methods: miR-384 levels within GC and matched non-tumor tissues were determined through RT-qPCR. GC cells underwent miR-384 mimic or inhibitor transfection to investigate cell proliferation, invasion and EMT. Bioinformatic analysis was conducted to predict miR-384’s target mRNA. Also, rescued experiments were carried out for verifying targeted binding of miR-384 to CTNNB1. Furthermore, we conducted in vivo experiments for analyzing the effect of miR-384. Results: miR-384 expression declined within GC tumor tissue and cells. MiR-384 inhibited GC cell growth and migration while promoting their apoptosis. From bioinformatics analysis, we found that miR-384 targeted CTNNB1. MiR-384 inhibits the expression and nuclear translocation of CTNNB1, and regulated EMT and proliferation of GC cells. Moreover, miR-384 was targeting CTNNB1 inhibited GC tumor growth. Conclusion: miR-384 suppresses GC cell proliferation and EMT progress, and enhances their apoptosis via CTNNB1.