Knockdown of long non-coding RNA HOTAIR inhibits malignant biological behaviors of human glioma cells via modulation of miR-326

// Jing Ke 1, 2 , Yi-long Yao 3 , Jian Zheng 3 , Ping Wang 1, 2 , Yun-hui Liu 3 , Jun Ma 1, 2 , Zhen Li 3 , Xiao-bai Liu 3 , Zhi-qing Li 1, 2 , Zhen-hua Wang 4 , Yi-xue Xue 1, 2 1 Department of Neurobiology, College of Basic Medicine, China Medical University, Shenyang 110122, China 2 Institute of Pathology and Pathophysiology, China Medical University, Shenyang 110122, China 3 Department of Neurosurgery, Shengjing Hospital of China Medical University, Shenyang 110004, China 4 Department of Physiology, College of Basic Medicine, China Medical University, Shenyang 110122, China Correspondence to: Yi-xue Xue, e-mail: xueyixue888@163.com Keywords: lncRNA, HOTAIR, miR-326, glioma, FGF1 Received: February 07, 2015      Accepted: June 17, 2015      Published: June 27, 2015 ABSTRACT Glioma is the most common and aggressive primary adult brain tumor. Long non-coding RNAs (lncRNAs) have important roles in a variety of biological properties of cancers. Here, we elucidated the function and the possible molecular mechanisms of lncRNA HOTAIR in human glioma U87 and U251 cell lines. Quantitative RT-PCR demonstrated that HOTAIR expression was up-regulated in glioma tissues and cell lines. Knockdown of HOTAIR exerted tumor-suppressive function in glioma cells. Further, HOTAIR was confirmed to be the target of miR-326 and miR-326 mediated the tumor-suppressive effects of HOTAIR knockdown on glioma cell lines. Moreover, over-expressed miR-326 reduced the FGF1 expression which played an oncogenic role in glioma by activating PI3K/AKT and MEK 1/2 pathways. In addition, the in vivo studies also supported the above findings. Taken together, knockdown of HOTAIR up-regulated miR-326 expression, and further inducing the decreased expression of FGF1, these results provided a comprehensive analysis of HOTAIR-miR-326-FGF1 axis in human glioma and provided a new potential therapeutic strategy for glioma treatment.