MicroRNA‑1288 promotes cell proliferation of human glioblastoma cells by repressing ubiquitin carboxyl‑terminal hydrolase CYLD expression.
Jun Yin, Chengyin Weng, Jieke Ma, Fanfan Chen, Yecai Huang, Mei Feng
Author Information
Jun Yin: 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.
Chengyin Weng: Department of Oncology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
Jieke Ma: Department of Craniofacial and Neurosurgery, Sichuan Cancer Hospital, Chengdu, Sichuan 610041, P.R. China.
Fanfan Chen: Department of Neurosurgery, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, Guangdong 510180, P.R. China.
Yecai Huang: 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.
Mei Feng: 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.
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 prolife-ration, 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.
References
Oncol Lett. 2016 Oct;12 (4):3021-3027
[PMID: 27698893]
