Oncotarget

Research Papers:

Long non-coding RNA NEAT1 regulates epithelial membrane protein 2 expression to repress nasopharyngeal carcinoma migration and irradiation-resistance through miR-101-3p as a competing endogenous RNA mechanism

Yujia Wang, Chunting Wang, Can Chen, Fengbo Wu, Pengfei Shen, Peng Zhang _, Gu He and Xiang Li

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Oncotarget. 2017; 8:70156-70171. https://doi.org/10.18632/oncotarget.19596

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Abstract

Yujia Wang1,*, Chunting Wang1,2,*, Can Chen3, Fengbo Wu1, Pengfei Shen1, Peng Zhang2, Gu He1 and Xiang Li1

1Department of Urology and State Key Laboratory of Biotherapy, West China Hospital, West China Medical School, Sichuan University, Chengdu 610041, P.R. China

2Department of Radiation Oncology, Sichuan Cancer Hospital & Institute, Sichuan Cancer Center, School of Medicine, University of Electronic Science and Technology of China, Chengdu 610041, P.R. China

3School of Pharmacy, Chengdu Medical College, Chengdu 611137, P.R. China

*These authors have contributed equally to this work

Correspondence to:

Peng Zhang, email: [email protected]

Gu He, email: [email protected]

Xiang Li, email: [email protected]

Keywords: NEAT1, EMP2, miR-101-3p, nasopharyngeal carcinoma, sponge

Received: May 17, 2017     Accepted: June 29, 2017     Published: July 26, 2017

ABSTRACT

The altered expression of long non-coding RNAs (lncRNAs) is often related to carcinogenesis, metastasis and resistance to radiation or chemotherapy. In the current study, cDNA microarray analysis found that NEAT1 expression was reduced in nasopharyngeal carcinoma (NPC) patients and that it regulated NPC progression. However, the detailed mechanisms of NEAT1 in NPC were unclear. NEAT1 repressed NPC cell growth, invasion and radiation resistance in vitro and tumor metastasis in vivo. In addition, the results of an approach integrating bioinformatics, luciferase reporter assays and RNA immunoprecipitation indicated that NEAT1 antagonized miR-101-3p through a competing endogenous RNA (ceRNA) mechanism and that the interaction between NEAT1 and EMP2 was miR-101-3p dependent. Our results showed a novel connection of NEAT1, miR-101-3p and EMP2 in NPC migration and radiation resistance.


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