Oncotarget

Research Papers:

Long non-coding RNA MIAT promotes breast cancer progression and functions as ceRNA to regulate DUSP7 expression by sponging miR-155-5p

Tian Luan, Ximei Zhang, Shuyuan Wang, Yan Song, Shunheng Zhou, Jing Lin, Weiwei An, Weiguang Yuan, Yue Yang, Huilong Cai, Qingyuan Zhang and Lihong Wang _

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Oncotarget. 2017; 8:76153-76164. https://doi.org/10.18632/oncotarget.19190

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Abstract

Tian Luan1,*, Ximei Zhang2,*, Shuyuan Wang3, Yan Song1, Shunheng Zhou3, Jing Lin1, Weiwei An1, Weiguang Yuan1, Yue Yang1, Huilong Cai1, Qingyuan Zhang1,4 and Lihong Wang1,5

1Institute of Cancer Prevention and Treatment, Heilongjiang Academy of Medical Science, Harbin Medical University, Harbin 150081, China

2Department of Histology and Embryology, Harbin Medical University, Harbin 150081, China

3College of Bioinformatics Science and Technology, Harbin Medical University, Harbin 150081, China

4Department of Internal Medicine, The Third Affiliated Hospital of Harbin Medical University, Harbin 150081, China

5Department of Pathophysiology, School of Medicine, Southeast University, Nanjing 210009, China

*These authors have contributed equally to this work

Correspondence to:

Lihong Wang, email: [email protected]

Qingyuan Zhang, email: [email protected]

Keywords: MIAT, breast cancer, ceRNA, miR-155-5p, DUSP7

Received: December 20, 2016     Accepted: June 19, 2017     Published: July 12, 2017

ABSTRACT

Long non-coding RNAs (lncRNA) have been reported as key regulators in the progression and metastasis of breast cancer. In this study, we found that the lncRNA myocardial infarction associated transcript (MIAT) expression was upregulated in breast cancer in The Cancer Genome Atlas (TCGA) data sets. We validated that MIAT was higher in breast cancer cell lines and advanced breast tumors than in normal controls. And MIAT overexpression associated with TNM stage and lymphnode metastasis. Knockdown MIAT inhibited breast cancer cell proliferation and promoted apoptosis. Also MIAT downregulation suppressed epithelial-mesenchymal transition (EMT) and decreased migration and invasion in MDA-MB-231 and MCF-7 breast cancer cell lines. More importantly, knockdown MIAT inhibited tumor growth in vivo. Our results suggested that MIAT acted as a competing endogenous RNA (ceRNA) to regulate the expression of dual specificity phosphatase 7 (DUSP7) by taking up miR-155-5p in breast cancer. There were positive correlation between MIAT and DUSP7 expression in breast cancer patients. We conclude that MIAT promotes breast cancer progression and functions as ceRNA to regulate DUSP7 expression by sponging miR-155-5p in breast cancer.


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