Abstract
Retinoblastoma (RB) represents an aggressive malignancy in the eye during the period of infancy and childhood. We delineated the ability of microRNA-186 (miR-186) to influence viability, invasion, migration, angiogenesis, and apoptosis of RB via the Hedgehog signaling pathway by targeting AAA domain-containing protein 2 (ATAD2). The microarray-based analysis was adopted to identify differentially expressed genes (DEGs) related to RB. Subsequently, RB cells were treated with miR-186 mimic, miR-186 inhibitor, or si-ATAD2. The expression of miR-186, ATAD2, Hedgehog signaling pathway-related genes were evaluated, and the target relationship between miR-186 and ATAD2 was verified. Finally, cell proliferation, invasion, migration, apoptosis, and angiogenesis were assessed. ATAD2 was identified as a DEG and modulated by miR-186. Moreover, we revealed that ATAD2 was highly expressed, whereas miR-186 was lowly expressed, and the Hedgehog signaling pathway was activated in RB. Then, ATAD2 as a putative target of miR-186 was validated using a luciferase assay. miR-186 mimic or siRNA-ATAD2 in RB cells reduced cell viability, invasion, and migration coordinating with elevated apoptosis via impairing the Hedgehog signaling pathway, where repressed angiogenesis was observed. Overexpression of miR-186 attenuates RB via the inactivation of the Hedgehog signaling pathway by downregulating ATAD2.