Current Chemical Genomics and Translational Medicine




(Discontinued)

ISSN: 2213-9885 ― Volume 12, 2018
RESEARCH ARTICLE

MiR-9 Promotes Apoptosis Via 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, *, Jing Zheng1, *
1 Shanghai Key Laboratory of New Drug Design, School of Pharmacy, East China University of Science and Technology, Shanghai 200237, China
2 Center for Medical Research and Innovation, Shanghai Pudong Hospital, Fudan University Pudong Medical Center, 2800 Gongwei Road, Pudong, Shanghai 201399, China

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.


Article Information


Identifiers and Pagination:

Year: 2017
Volume: 11
First Page: 31
Last Page: 40
Publisher Id: CCGTM-11-31
DOI: 10.2174/2213988501711010031

Article History:

Received Date: 05/02/2017
Revision Received Date: 01/05/2017
Acceptance Date: 22/05/2017
Electronic publication date: 31/07/2017
Collection year: 2017

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© 2017 Zu et al.

open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: (https://creativecommons.org/licenses/by/4.0/legalcode). This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.


* 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, jjfu@ecust.edu.cn, zhangpg@yahoo.com


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