ANRIL acts as onco-lncRNA by regulation of microRNA-24/c-Myc, MEK/ERK and Wnt/β-catenin pathway in retinoblastoma.

Retinoblastoma is the most common intraocular malignant tumor in infants and children with metastatic potential. This study aimed to investigate the effects of antisense non-coding RNA in the INK4 locus (ANRIL) on retinoblastoma cell viability, migration and invasion, as well as the potential downstream molecules and possible signaling pathways. We found that ANRIL was highly expressed in retinoblastoma tissues and cells. Overexpression of ANRIL promoted the viability, migration and invasion of retinoblastoma Y79 cells and retinal pigment epithelial ARPE-19 cells, as well as activated MEK/ERK and Wnt/β-catenin pathways. Suppression of ANRIL had opposite effects. Moreover, ANRIL negatively regulated the expression of miR-24, which played tumor suppressive roles in retinoblastoma cells. Furthermore, ANRIL positively regulated the expression of c-Myc, which was a target gene of miR-24 in retinoblastoma cells. In Conclusion, Our research verified the oncogenic roles of ANRIL in retinoblastoma. Overexpression of ANRIL promoted viability, migration and invasion of retinoblastoma cells by activating MEK/ERK and Wnt/β-catenin pathways, as well as down-regulating miR-24 and then up-regulating c-Myc.