Wei Li1, Junmei Wang2, Dongqing Zhang3, Xiting Zhang4, Jumei Xu5, Li Zhao6. 1. Department of Ophthalmology, Jining No.1 People's Hospital, Jining, Shandong, China. 2. Department of Clinical Laboratory, Rizhao Hospital of TCM, Rizhao, Shandong, China. 3. Department of Public Health, The People's Hospital of Zhangqiu Area, Jinan, Shandong, China. 4. Department of Ward, The People's Hospital of Zhangqiu Area, Jinan, Shandong, China. 5. Department of Hepatobiliary Gastrointestinal, The People's Hospital of Zhangqiu Area, Jinan, Shandong, China. 6. Department of Ophthalmology, Yankuang New Journey General Hospital, Zoucheng, Shandong, China.
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.
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 humanRB. 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.