miR-133b inhibits glioma cell proliferation and invasion by targeting Sirt1.

TLDR: Light is shed on the regulatory mechanism of miR-133b in glioma growth and metastasis via direct mediation of Sirt1 expression, and it is suggested that Sirt 1 may serve as a potential therapeutic target forglioma.

Abstract: // Chuntao Li 1 , Zhixiong Liu 1 , Kui Yang 1 , Xin Chen 1 , Yu Zeng 1 , Jinfang Liu 1 , Zhenyan Li 1 , Yunsheng Liu 1 1 Department of Neurosurgery, Xiangya Hospital of Central South University, Changsha, 410008 Hunan, China Correspondence to: Zhixiong Liu, email: zxliu_csu@sina.com Keywords: glioma, microRNA-133b, silent information regulator 1, proliferation, invasion Received: November 16, 2015      Accepted: April 16, 2016      Published: May 06, 2016 ABSTRACT MicroRNAs (miRs) are a class of small non-coding RNAs that function as mediators of gene expression. Dysregulations of miRs have been implicated in the development and progression of glioma. In the present study, we investigated the role of miR-133b in mediating the proliferation and invasion of glioma cells, and the potential mechanism. Real-time RT-PCR results showed that miR-133b expression was significantly decreased in glioma tissues compared with normal brain tissues. Luciferase reporter assay further identified silent information regulator 1 (Sirt1) as a novel direct target of miR-133b in glioma U87 cells. Overexpression of miR-133b suppressed Sirt1 expression and reduced the proliferation and invasion of U87 cells, which could be partly rescued by forced expression of Sirt1. In addition, the Sirt1 mRNA level was significantly higher in glioma tissues than in normal brain tissues, and was inversely correlated with miR-133b level in glioma tissues. In summary, our study sheds light on the regulatory mechanism of miR-133b in glioma growth and metastasis via direct mediation of Sirt1 expression, and suggests that Sirt1 may serve as a potential therapeutic target for glioma.