Abstract
OBJECTIVE: This research attempts to clarify the function of miR-1287-5p in gastric cancer (GC) and the mechanisms that underlie it. METHODS: MiR-1287-5p and LAMTOR3 mRNA levels were determined using qRT-PCR.Western blot analysis was used to identify LAMTOR3 protein expression.The GC cells were assessed for proliferation, migration, invasion, and apoptosis using the CCK-8, wound-healing, transwell invasion assay, and flow cytometry tests, respectively.The dual-luciferase reporter assay was used to validate the miR-1287-5p target. RESULTS: GC had lower miR-1287-5p levels than normal cells or tissues.MiR-1287-5p over-expression dramatically reduced GC cell proliferation, migration, invasion, and accelerated apoptosis in contrast to the impact of miR-1287-5p knockdown.The dual-luciferase reporter experiment confirmed the direct targeting relationship between miR-1287-5p and LAMTOR3.Rescue experiments showed that GC cells proliferation, migration, invasion, and apoptosis caused by miR-1287-5p were all reversed by concurrent over-expression or down-regulation of LAMTOR3. CONCLUSIONS: This current study found that miR-1287-5p suppressed GC cells proliferation, migration, and invasion while increasing apoptosis by decreasing LAMTOR3 expression. This revealed that miR-1287-5p may function as a plausible therapeutic target or biomarker for GC.