Oncotarget

Research Papers:

LncRNA HOTAIR acts as competing endogenous RNA to control the expression of Notch3 via sponging miR-613 in pancreatic cancer

Huihua Cai, Jie Yao, Yong An, Xuemin Chen, Weibo Chen, Di Wu, Boyang Luo, Yong Yang, Yong Jiang, Donglin Sun and Xiaozhou He _

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Oncotarget. 2017; 8:32905-32917. https://doi.org/10.18632/oncotarget.16462

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Abstract

Huihua Cai1,*, Jie Yao2,*, Yong An1, Xuemin Chen1, Weibo Chen1, Di Wu1, Boyang Luo1, Yong Yang1, Yong Jiang1, Donglin Sun1, Xiaozhou He3

1Department of Hepatobiliary Surgery, The First People's Hospital of Changzhou, The Third Hospital Affiliated to Soochow University, Changzhou, Jiangsu, China

2Department of Hepatobiliary and Pancreatic Surgery, Northern Jiangsu People's Hospital, The Clinic Medical College of Yangzhou University, Yangzhou, Jiangsu, China

3Department of Urology, The First People's Hospital of Changzhou, The Third Hospital Affiliated to Soochow University, Changzhou, Jiangsu, China

*These authors contributed equally to this work

Correspondence to:

Xiaozhou He, email: chh20072077@sina.com

Donglin Sun, email: czyysdl@163.com

Keywords: pancreatic cancer, miR-613, HOTAIR, cell proliferation, invasion and migration

Received: February 10, 2017     Accepted: March 11, 2017     Published: March 22, 2017

ABSTRACT

Pancreatic cancer is one of the most deadly cancers with a poor prognosis. Though studies have implicated the roles of microRNAs in pancreatic cancer progression, little is known about the role of miR-613 in pancreatic cancer. In the present study, the expression of miR-613 was down-regulated in pancreatic cancer tissues and cancer cell lines. Down-regulation of miR-613 was positively correlated with tumor differentiation, advanced TNM stage, nodal metastasis and shorter overall survival in patients with pancreatic cancer. Overexpression of miR-613 suppressed cell proliferation, invasion and migration, and induced cell apoptosis and cell cycle arrest at G0/G1 phase in pancreatic cancer cells. Bioinformatics analysis, luciferase reporter assay and rescue experiments showed that notch3 was a direct target of miR-613. MiR-613 was inversely correlated with notch3 expression in pancreatic cancer tissues. The long non-coding RNA, HOX transcript antisense RNA (HOTAIR) was up-regulated in both pancreatic cancer tissues and cancer cell lines, and HOTAIR suppressed the expression of miR-613 via functioning as a competing endogenous RNA. In vivo studies showed that stable overexpression of miR-613 or knock-down of HOTAIR suppressed tumor growth and also reduced the expression of notch3. In conclusion, these results suggest that HOTAIR functions as a competing endogenous RNA to regulate notch3 expression via sponging miR-613 in pancreatic cancer.


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