MiR-552-3p facilitated cell proliferation, migration and invasion by sponging Fibulin 5 in non-small cell lung cancer via activation of ERK/GSK3β/β-catenin signaling pathway

Abstract

Apart from the fact that miR-552-3p is known to promote cell progression among various cancers, its function on non-small cell lung cancer (NSCLC) is unknown which therefore emerges as the purpose of this research. TargetScan, Starbase, miRWalk, miRDB and the Cancer Genome Atlas Lung Adenocarcinoma (TCGA-LUAD) were utilized to analyze the target genes of miR-552-3p. NSCLC cells were transfected with miR-552-3p mimic, miR-552-3p inhibitor, Fibulin 5 (FBLN5) overexpression plasmid, and small interfering FBLN5 (siFBLN5) and treated with extracellular regulated protein kinases (ERK) pathway inhibitor PD98059. MiR-552-3p, FBLN5, p-ERK, ERK, p-glycogen synthase kinase 3β (GSK3β) and β-catenin levels were detected through quantitative reverse transcription-polymerase chain reaction and western blot. The binding sites between miR-552-3p and FBLN5 were predicted by TargetScan, which was tested through dual luciferase reporter analysis. Cell viability, migration and invasion were determined by cell counting kit-8 (CCK-8) assay, wound healing assay and transwell assay, respectively. MiR-552-3p expression was upregulated in NSCLC and FBLN5 functioned as its target. MiR-552-3p mimic promoted proliferation, migration, invasion, p-ERK, p-GSK3β and β-catenin expressions in NSCLC cells while miR-552-3p inhibitor did the opposite. Overexpressed FBLN5 suppressed proliferation, migration, invasion, p-ERK, p-GSK3β and β-catenin expressions in NSCLC cells whereas siFBLN5 exerted the effects opposite to overexpressed FBLN5. PD98059 enhanced the effect of overexpressed FBLN5 on NSCLC cell migration and invasion while reversing the effect of siFBLN5. MiR-552-3p facilitated cell proliferation, migration and invasion in NSCLC through sponging FBLN5 via activation of ERK/GSK3β/β-catenin pathway.