{"title":"MicroRNA-98通过介导Wnt/β-catenin通路，靶向HMGA2抑制视网膜母细胞瘤的发生发展。","authors":"Wei Li, Junmei Wang, Dongqing Zhang, Xiting Zhang, Jumei Xu, Li Zhao","doi":"10.3233/CBM-182315","DOIUrl":null,"url":null,"abstract":"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>MiR-98 targets HMGA2 to act as a tumor suppressor in RB by mediating Wnt/β-catenin pathway.</p>","PeriodicalId":520578,"journal":{"name":"Cancer biomarkers : section A of Disease markers","volume":" ","pages":"79-88"},"PeriodicalIF":1.9000,"publicationDate":"2019-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3233/CBM-182315","citationCount":"13","resultStr":"{\"title\":\"MicroRNA-98 targets HMGA2 to inhibit the development of retinoblastoma through mediating Wnt/β-catenin pathway.\",\"authors\":\"Wei Li, Junmei Wang, Dongqing Zhang, Xiting Zhang, Jumei Xu, Li Zhao\",\"doi\":\"10.3233/CBM-182315\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Background: </strong>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.</p><p><strong>Methods: </strong>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.</p><p><strong>Results: </strong>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.</p><p><strong>Conclusion: </strong>MiR-98 targets HMGA2 to act as a tumor suppressor in RB by mediating Wnt/β-catenin pathway.</p>\",\"PeriodicalId\":520578,\"journal\":{\"name\":\"Cancer biomarkers : section A of Disease markers\",\"volume\":\" \",\"pages\":\"79-88\"},\"PeriodicalIF\":1.9000,\"publicationDate\":\"2019-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.3233/CBM-182315\",\"citationCount\":\"13\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Cancer biomarkers : section A of Disease markers\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.3233/CBM-182315\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Cancer biomarkers : section A of Disease markers","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.3233/CBM-182315","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
MicroRNA-98 targets HMGA2 to inhibit the development of retinoblastoma through 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 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.
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