Circular RNA circ_0000034 upregulates STX17 level to promote human retinoblastoma development via inhibiting miR-361-3p

Objective Retinoblastoma (RB) is a common intraocular tumor of infancy and childhood. Circular RNAs (circRNAs) are related to the development of RB. The purpose of this research was to reveal the functional mechanism of circRNA circ_0000034 in RB. Materials and methods Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) and Western blot were applied to determine the levels of genes. MTT assay and flow cytometry were employed to assess cell proliferation and apoptosis rate, respectively. Furthermore, cell migratory and invasive abilities were measured using the transwell assay. Mouse xenograft was conducted to analyze the effect of circ_0000034 on tumor growth in vivo. Besides, the interaction between miR-361-3p and circ_0000034 or syntaxin 17 (STX17) was predicted by starBase, and then, confirmed by the Dual-Luciferase reporter assay and RNA immunoprecipitation (RIP) assay. Results The levels of circ_0000034 and STX17 were increased and miR-361-3p level was decreased in RB tissues and cells. Circ_0000034 knockdown suppressed cell proliferation, migration, invasion, autophagy, and tumor growth, and induced apoptosis in RB. Circ_0000034 targeted miR-361-3p and miR-361-3p bound to STX17. Circ_0000034 overexpression and miR-361-3p knockdown reversed the effect of miR-361-3p upregulation and STX17 depletion on the growth of RB cells, respectively. Besides, circ_0000034 elevated STX17 level by repressing miR-361-3p expression. Conclusions We demonstrated that circ_0000034 knockdown suppressed the development of RB by the modulation of miR-361-3p/STX17 axis. Our findings provided a theoretical basis for the treatment of RB.