Oncotarget

Research Papers:

Long non-coding RNA TUG1 promotes endometrial cancer development via inhibiting miR-299 and miR-34a-5p

Lifen Liu, Xin Chen, Ying Zhang, Yanrong Hu, Xiaoqing Shen and Weipei Zhu _

PDF  |  HTML  |  Supplementary Files  |  How to cite

Oncotarget. 2017; 8:31386-31394. https://doi.org/10.18632/oncotarget.15607

Metrics: PDF 1717 views  |   HTML 2985 views  |   ?  


Abstract

Lifen Liu1, Xin Chen1, Ying Zhang1, Yanrong Hu1, Xiaoqing Shen1 and Weipei Zhu1

1Department of Gynecology and Obstetrics, The Second Affiliated Hospital of Soochow University, Suzhou 215004, Jiangsu, China

Correspondence to:

Weipei Zhu, email: [email protected]

Keywords: lincRNA, endometrial cancer

Received: October 20, 2016    Accepted: January 24, 2017    Published: February 22, 2017

ABSTRACT

It is generally known that the human genome makes a large amount of noncoding RNAs compared with coding genes. Long non-coding RNAs (lncRNAs) which composed of more than 200 nucleotides have been described as the largest subclass of the non-coding transcriptome in human noncoding RNAs. Existing research shows that lncRNAs exerted biological functions in various tumors via participating in both oncogenic and tumor suppressing pathways. The previous studies indicated that lncRNA taurine upregulated 1 (TUG1) play important roles in the initiation and progression of malignancies. In this study,based on previous research, we investigated the expression and biological role of the lncRNA-TUG1. We analyzed the relationship between lncRNA-TUG1and endometrial carcinoma (EC) in a total 104 EC carcinoma specimens, compared with that in normal tissues. We found that lncRNA-TUG1 expression in cancer tissues was significantly higher than that in adjacent tissues. Through a series of experiments, the results demonstrated that lncRNA-TUG1 enhances the evolution and progression of EC through inhibiting miR-299 and miR-34a-5p.


Creative Commons License All site content, except where otherwise noted, is licensed under a Creative Commons Attribution 4.0 License.
PII: 15607