MicroRNA-98 targets HMGA2 to inhibit the development of retinoblastoma through mediating Wnt/β-catenin pathway.

Abstract

Background: Recently, the incidence and mortality of retinoblastoma (RB) have gradually increased. Many studies support the pivotal role of microRNAs (miRNAs) in the pathogenesis of RB. Alternation of microRNA-98 (miR-98) expression has been detected in several cancers, excluding RB. This study was designed to assess the regulatory mechanisms of miR-98 in human RB.

Methods: RT-qPCR and Western blot analysis were used to detect miR-98 and HMGA2 expression. The effects of miR-98 were explored using the CCK-8 and Transwell assays. Dual-luciferase reporter assay was performed to confirm the relationship between miR-98 and HMGA2.

Results: In RB, downregulation of miR-98 was identified. Upregulation of miR-98 inhibited proliferation, invasion and migration of RB cells. Further, HMGA2 was confirmed as a direct target gene of miR-98. And knockdown of HMGA2 suppressed the progression of RB. Moreover, upregulation of HMGA2 reversed the suppressive effects in the development of RB. In addition, miR-98 also showed suppressive effect on EMT and Wnt/β-catenin pathway.

Conclusion: MiR-98 targets HMGA2 to act as a tumor suppressor in RB by mediating Wnt/β-catenin pathway.