Oncotarget

Research Papers:

The long non-coding RNA SNHG14 inhibits cell proliferation and invasion and promotes apoptosis by sponging miR-92a-3p in glioma

Qiang Wang _, Yiwan Teng, Rong Wang, Danni Deng, Yijie You, Ya Peng, Naiyuan Shao and Feng Zhi

PDF  |  HTML  |  How to cite  |  Order a Reprint

Oncotarget. 2018; 9:12112-12124. https://doi.org/10.18632/oncotarget.23960

Metrics: PDF 1120 views  |   HTML 1288 views  |   ?  


Abstract

Qiang Wang1,*, Yiwan Teng2,*, Rong Wang3, Danni Deng3, Yijie You1, Ya Peng1, Naiyuan Shao1 and Feng Zhi1,3

1Department of Neurosurgery, The First People’s Hospital of Changzhou, Changzhou, Jiangsu, China

2Changzhou Center for Biotech Development, Changzhou, Jiangsu, China

3Modern Medical Research Center, The Third Affiliated Hospital of Soochow University, Changzhou, Jiangsu, China

*These authors contributed equally to this work

Correspondence to:

Ya Peng, email: neuropengya@sina.com

Naiyuan Shao, email: naiyuanshao@126.com

Feng Zhi, email: danielzhif@suda.edu.cn

Keywords: SNHG14; miR-92a-3p; glioma; prolifertion; invasion

Received: July 29, 2017     Accepted: November 16, 2017     Published: January 04, 2018

ABSTRACT

Malignant glioma is one of the most common types of primary brain tumours. Long non-coding RNAs (lncRNAs) have recently emerged as a new class of therapeutic targets for many cancers. In this study, we aimed to explore the functional involvement of small nucleolar RNA host gene 14 (SNHG14) and its potential regulatory mechanism in glioma progression. SNHG14 was found to be downregulated in human glioma tissues and cell lines. SNHG14 significantly inhibited cell viability, reduced cell invasion, and induced apoptosis in glioma cell lines. Furthermore, a correlation analysis demonstrated that there was a negative correlation between SNHG14 expression and miR-92a-3p expression. Bioinformatics prediction and luciferase reporter assays demonstrated that miR-92a-3p could directly bind to SNHG14. miR-92a-3p was significantly upregulated in glioma and acted as an oncogene in glioma cells by inhibiting Bim. Moreover, mechanistic investigations showed that miR-92a-3p could reverse the tumour suppressive effects induced by SNHG14 in glioma, indicating that SNHG14 may act as an endogenous sponge that competes for binding to miR-92a-3p. Our results suggest that SNHG14 and miR-92a-3p may be promising molecular targets for glioma therapy.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 3.0 License.
PII: 23960