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MicroRNA-300 inhibited glioblastoma progression through ROCK1

Fucheng Zhou, Yang Li, Zhen Hao, Xuanxi Liu, Liang Chen, Yu Cao, Zuobin Liang, Fei Yuan, Jie Liu, Jianjiao Wang, Yongri Zheng, Deli Dong, Shan Bian, Baofeng Yang, Chuanlu Jiang and Qingsong Li _

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Oncotarget. 2016; 7:36529-36538. https://doi.org/10.18632/oncotarget.9068

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Fucheng Zhou1,*, Yang Li1,*, Zhen Hao1, Xuanxi Liu1, Liang Chen1, Yu Cao1, Zuobin Liang1, Fei Yuan1, Jie Liu1, Jianjiao Wang1, Yongri Zheng1, Deli Dong2, Shan Bian3, Baofeng Yang2, Chuanlu Jiang1, Qingsong Li1

1Department of Neurosurgery, The 2nd Affiliated Hospital, Harbin Medical University, Harbin 150086, China

2Harbin Medical University, Harbin 150086, China

3Institute of Molecular Biology, Austrian Academy of Sciences, Vienna, Austria

*These authors have contributed equally to this work

Correspondence to:

Qingsong Li, email: [email protected]

Chuanlu Jiang, email: [email protected]

Baofeng Yang, email: [email protected]

Keywords: glioblastoma, microRNAs, miR-300, ROCK1

Received: September 06, 2015    Accepted: March 06, 2016    Published: April 28, 2016


Glioblastoma is a common type of brain aggressive tumors and has a poor prognosis. MicroRNAs (miRNAs) are a class of small, endogenous and non-coding RNAs that play crucial roles in cell proliferation, survival and invasion. Deregulated expression of miR-300 has been studied in a lot of cancers. However, the role of miR-300 in glioblastoma is still unknown. In this study, we demonstrated that miR-300 expression was downregulated in glioblastoma tissues compared with the normal tissues. Lower expression level of miR-300 was observed in thirty cases (75 %, 30/40) of glioblastoma samples compared with the normal samples. Moreover, the overall survival of glioblastoma patients with lower miR-300 expression level was shorter than those with higher miR-300 expression level. In addition, miR-300 expression was also downregulated in glioblastoma cell lines. Overexpression of miR-300 inhibited cell proliferation, cell cycle and invasion in glioblastoma cell line U87 and U251. Moreover, we identified ROCK1 as a direct target of miR-300 in U87 and U251 cells. Overexpression of ROCK1 partially rescued the miR-300-mediated cell growth. ROCK1 expression levels in glioblastoma tissues were higher than that in normal tissues. ROCK1 expression levels were higher in thirty-one cases of glioblastoma samples than their normal samples. Furthermore, the expression level ROCK1 was inversely correlated with the expression level of miR-300. Importantly, overexpression of miR-300 suppressed glioblastoma progression in an established xenograft model. In conclusion, we revealed that miR-300 might act as a tumor suppressor gene through inhibiting ROCK1 in glioblastoma.

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