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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-...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2017
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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 |
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. |
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