Oncotarget

Research Papers:

Long non-coding RNA HOXA-AS2 promotes proliferation and invasion of breast cancer by acting as a miR-520c-3p sponge

Yu Fang, Jingxuan Wang, Feng Wu, Ying Song, Shu Zhao and Qingyuan Zhang _

PDF  |  HTML  |  How to cite

Oncotarget. 2017; 8:46090-46103. https://doi.org/10.18632/oncotarget.17552

Metrics: PDF 1858 views  |   HTML 3580 views  |   ?  


Abstract

Yu Fang1, Jingxuan Wang1, Feng Wu2, Ying Song1, Shu Zhao1 and Qingyuan Zhang1

1Department of Medical Oncology, The Affiliated Tumor Hospital of Harbin Medical University, Nangang District, Harbin 151000, Heilongjiang Province, China

2Department of Gastroenterology, The First Affiliated Hospital of Harbin Medical University, Nangang District, Harbin 151000, Heilongjiang Province, China

Correspondence to:

Qingyuan Zhang, email: [email protected]

Keywords: LncRNA-HOXA-AS2, miR-520c-3p, breast cancer, growth, metastasis

Received: January 16, 2017    Accepted: March 01, 2017    Published: May 02, 2017

ABSTRACT

The long non-coding RNA (lncRNA) HOXA cluster antisense RNA2 (HOXA-AS2) has recently been shown to be dysregulated and involved in the progression of several cancers. However, the biological role and clinical significance of HOXA-AS2 in the carcinogenesis of breast cancer are still unclear. In the present study, we found that HOXA-AS2 was up-regulated in human breast cancer tissues and cell lines and associated with clinicopathological characteristics. Silencing of HOXA-AS2 inhibited the progression of breast cancer cells in vitro and in vivo. Furthermore, microarray profiling indicated that HOXA-AS2 serves as an endogenous sponge by directly binding to miR-520c-3p and down-regulating miR-520c-3p expression. We demonstrated that HOXA-AS2 controls the expression of miR-520c-3p target genes, TGFBR2 and RELA, in breast cancer cells. Therefore, our study may provide a better understanding of the pathogenesis of breast cancer and suggests that HOXA-AS2 may be a potential prognostic and therapeutic target in breast cancer.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 17552