Current Chemical Genomics and Translational Medicine

2017, 11 : 31-40
Published online 2017 July 31. DOI: 10.2174/2213988501711010031
Publisher ID: CCGTM-11-31

RESEARCH ARTICLE
MiR-9 Promotes Apoptosis Suppressing SMC1A Expression in GBM Cell Lines

Yong Zu1 , Zhichuan Zhu1 , Min Lin1 , Dafeng Xu1 , Yongjun Liang2 , Yueqian Wang2 , Zhengdong Qiao2 , Ting Cao2 , Dan Yang2 , Lili Gao2 , Pengpeng Jin2 , Peng Zhang2, * , Jianjun Fu1, * and Jing Zheng1, *

* Address correspondence to these authors at No. 130, Meilong Road, Shanghai 200237; 2800 Gongwei Road, Pudong, Shanghai 201399, P.R. China, Tel: +86-21-64252293; E-mails: , , zhengjing@ecust.edu.cn

ABSTRACT

Objective:

Glioblastomas multiforme (GBM) is the most malignant brain cancer, which presented vast genomic variation with complicated pathologic mechanism.

Method:

MicroRNA is a delicate post-transcriptional tuner of gene expression in the organisms by targeting and regulating protein coding genes. MiR-9 was reported as a significant biomarker for GBM patient prognosis and a key factor in regulation of GBM cancer stem cells. To explore the effect of miR-9 on GBM cell growth, we over expressed miR-9 in U87 and U251 cells. The cell viability decreased and apoptosis increased after miR-9 overexpression in these cells. To identify the target of miR-9, we scanned miR-9 binding site in the 3’UTRs region of expression SMC1A (structural maintenance of chromosomes 1A) genes and designed a fluorescent reporter assay to measure miR-9 binding to this region. Our results revealed that miR-9 binds to the 3’sUTR region of SMC1A and down-regulated SMC1A expression.

Result:

Our results indicated that miR-9 was a potential therapeutic target for GBM through triggering apoptosis of cancer cells.

Keywords:

GBM, miR-9, SMC1A, U87, U251, apoptosis.