Polymer nanoparticle delivery of microRNA-1303 suppresses renal cell carcinoma differentiation via regulation of small nucleolar RNA host gene 16

Abstract

Small nucleolar RNA host gene 16 (SNHG16) participates in some cancers as microRNA (miR)-1303 is also reported to function on proliferation of various cancer cells. This study aimed to assess SNHG16 and miR-1303′s role in renal cell carcinoma (RCC) and its underlying mechanism. RT-qPCR was used to determine SNHG16 and miR-1303 expression in RCC cells (A498, 786-O, ACHN and OS-RC-2) and normal kidney epithelial cells (HK-2). Functional experiment was established to detect the role of miR-1303. After synthesis of nanoparticles carrying miR-1303 and transfection, CCK-8 method and assays were used to evaluate cell growth and apoptosis. The target genes for miR-1303 were predicted using bioinformatics software, and binding of miR-1303 to SNHG16 was evaluated using the dual-luciferase reporter assay. miR-1303 was lowly expressed in RCC cells, with lowest level in A498 (p < 0.05). Overexpressed miR-1303 significantly reduced proliferation ability of RCC cells and induced apoptosis (p < 0.05). Besides, transfection of NP carrying miR-1303 mimic resulted in dramatically decreased migrated cells when reducing the expression of SNHG18 mRNA. The presence of NPs strengthened the inhibitory effect of miR-1303 on RCC. Furthermore, the miR-1303+SNHG16-WT co-transfection group had lower relative luciferase activity compared with miR-1303+SNHG16-MUT co-transfection group (p < 0.05). miR-1303 was down-regulated in RCC and NP delivery of miR-1303 inhibited RCC cell proliferation and differentiation through regulation of SNHG16. These findings suggest miR-1303 may become a potential molecular target for RCC.