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

Yin,Jun; Weng,Chengyin; Ma,Jieke; Chen,Fanfan; Huang,Yecai; Feng,Mei

doi:10.3892/mmr.2017.7481

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

Authors:
- Jun Yin
- Chengyin Weng
- Jieke Ma
- Fanfan Chen
- Yecai Huang
- Mei Feng
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Affiliations: Department of Radiation Oncology, Sichuan Cancer Hospital and Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu, Sichuan 610041, P.R. China, Department of Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China, Department of Craniofacial and Neurosurgery, Sichuan Cancer Hospital, Chengdu, Sichuan 610041, P.R. China, Department of Neurosurgery, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China
Published online on: September 13, 2017 https://doi.org/10.3892/mmr.2017.7481
Pages: 6764-6770
Copyright: © Yin et al. This is an open access article distributed under the terms of Creative Commons Attribution License.

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Abstract

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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