FAM64A antagonizes tumor suppressive effects of miR-610 in neuroblastoma in vitro.

BACKGROUND Due to the clinical heterogeneity, the mechanism involved in progression of neuroblastoma (NB) is so complex that no biomarker has been used in clinical treatment and diagnosis. In this study, we aimed to identify novel candidate biomarkers for precise therapy and diagnosis in NB. METHODS All the gene and miRNA expression data of NB were downloaded from Gene Expression Omnibus (GEO). Kaplan-Meier (KM) analysis was used to evaluate prognostic value of FAM64A in NB. Three online tools miRanda, miRWalk and TargetScan were applied to predict regulatory miRNAs of FAM64A. Cell counting kit-8 (CCK-8) and apoptosis assays were used to analyze biological behaviors of NB cell lines including SK-N-SH and SH-SY5Y. RESULTS In our study, we detected that FAM64A was up-regulated in NB tissues and cells compared to the normal samples. FAM64A high-expression was remarkably associated with the worse survival of NB patients. Remarkably, FAM64A was predicted to be directly regulated by miR-610, which was further confirmed by dual-luciferase reporter assay. Besides, overexpression of miR-610 hindered NB cell viability and facilitated cell apoptosis, whereas silencing miR-610 led to reverse results. Importantly, we classified that miR-610 functioned as a potential tumor suppressor in vitro that hindered growth and facilitated apoptosis of NB cells via targeting FAM64A. CONCLUSIONS Our investigation demonstrates that miR-610 is a promising novel biomarker for therapy and diagnosis of NB and shed a light on a novel clinical application of miR-610 for NB.