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MicroRNA-1288 promotes cell proliferation of human glioblastoma cells by repressing ubiquitin carboxyl-terminal hydrolase CYLD expression

Previous studies have demonstrated that microRNAs (miRs) are important regulators involved in various cancers, including human glioblastoma (GBM). However, the underlying mechanism of miR-1288 remains poorly understood, and its role in GBM has not been reported. The present study confirmed that miR-...

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Detalles Bibliográficos
Autores principales: Yin, Jun, Weng, Chengyin, Ma, Jieke, Chen, Fanfan, Huang, Yecai, Feng, Mei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5865833/
https://www.ncbi.nlm.nih.gov/pubmed/28901464
http://dx.doi.org/10.3892/mmr.2017.7481
Descripción
Sumario:Previous studies have demonstrated that microRNAs (miRs) are important regulators involved in various cancers, including human glioblastoma (GBM). However, the underlying mechanism of miR-1288 remains poorly understood, and its role in GBM has not been reported. The present study confirmed that miR-1288 expression was markedly upregulated in GBM. Ectopic expression of miR-1288 promoted the proliferation, colony formation and anchorage-independent growth of GBM cells. Bioinformatics analysis coupled with western blotting and luciferase report assays also indicated that miR-1288 promoted cell proliferation of GBM by targeting ubiquitin carboxyl-terminal hydrolase (CYLD). Knockdown of CYLD expression reversed the cell proliferation promotion by miR-1288-in in GBM. These results suggest that the miR-1288/CYLD axis may represent a potential therapeutic target for the treatment of GBM.