Hypermethylation of MEG3 promoter correlates with inactivation of MEG3 and poor prognosis in patients with retinoblastoma

Journal of Translational Medicine

Research

Jun Zhang¹  Yali Gao²  Peng Huang² 

[1] Department of Obstetrics and Gynecology, The Second Clinical Medical College (Shenzhen People’s Hospital), Jinan University, 518020, Shenzhen, People’s Republic of China;Department of Ophthalmology, The Second Clinical Medical College (Shenzhen People’s Hospital), Jinan University, 518020, Shenzhen, People’s Republic of China;

关键词: Retinoblastoma;    Long non-coding RNA;    MEG3;    Epigenetic;    DNA methylation;    Prognosis;   

DOI  :  10.1186/s12967-017-1372-8

 received in 2017-07-26, accepted in 2017-12-19,  发布年份 2017

来源: Springer

【 摘 要 】

BackgroundIn our previous study, we revealed that MEG3 was a tumor suppressor gene in retinoblastoma and inhibited proliferation of retinoblastoma cells by regulating the activity of the Wnt/β-catenin pathway. Here, we further explored the mechanism of MEG3 inactivation in retinoblastoma.MethodsMSP and qRT-PCR were performed to detect the methylation status of MEG3 promoter and levels of MEG3 expression, respective. To further explore relationship between MEG3 expression and epigenetic modifications, 5-Aza-CdR was used to interfere with DNA methylation. In addition, we evaluated proliferation, apoptosis and the expression of β-catenin via CCK-8, flow cytometric analysis and western blot analysis, respective.ResultsHypermethylation of MEG3 promoter was observed more frequently in retinoblastoma tissues and was highly associated with low MEG3 expression and poor survival of retinoblastoma patients. We also provided evidence demonstrating that hypermethylation of MEG3 promoter depressed MEG3 expression, promoted proliferation, inhibited apoptosis and increased β-catenin expression of retinoblastoma cells in vitro.ConclusionsOur present study indicates that promoter silencing by hypermethylation may account for the loss of MEG3 expression and predict poor prognosis.

【 授权许可】

CC BY   
© The Author(s) 2017