Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration. (15th January 2017)

• Record Type: Journal Article
• Authors: Hu, Yingying; Sun, Xiangwei; Mao, Chenchen; Guo, Gangqiang; Ye, Sisi; Xu, Jianfeng; Zou, Ruanmin; Chen, Jun; Wang, Ledan; Duan, Ping; Xue, Xiangyang
• Is Part Of: Cancer medicine. Volume 6:Number 2(2017:Feb.)
• Page Start: 471
• Page End: 482
• Publication Date: 2017-01-15
• Subjects: Bcl‐2 -- cervical cancer -- epithelial–mesenchymal transition -- LncRNA -- TUG1; 616.994005
• DOI: 10.1002/cam4.994
• Languages: English
• ISSNs: 2045-7634

Abstract

Abstract: Long noncoding RNAs (lncRNAs), a novel class of transcripts that have critical roles in carcinogenesis and progression, have emerged as important gene expression modulators. Recent evidence indicates that lncRNA taurine‐upregulated gene 1 (TUG1) functions as an oncogene in numerous types of human cancers. However, its function in the development of cervical cancer remains unknown. The aim of this research was to investigate the clinical significance and biological functions of TUG1 in cervical cancer. TUG1 was found to be significantly upregulated in cervical cancer tissues and four cervical cancer cell lines by quantitative real‐time polymerase chain reaction (qRT‐PCR). Elevated TUG1 expression was correlated with larger tumor size, advanced international federation of gynecology and obstetrics (FIGO) stage, poor differentiation, and lymph node metastasis. Furthermore, knockdown of TUG1 suppressed cell proliferation with activation of apoptosis, in part by regulating the expression of Bcl‐2 and caspase‐3. Silencing of TUG1 inhibited cell migration and invasion via the progression of epithelial–mesenchymal transition (EMT). Taken together, our findings indicate that TUG1 acts as an oncogene in cervical cancer and may represent a novel therapeutic target. Abstract : LncRNA TUG1 expression was significantly upregulated in cervical cancer and correlated with tumor size, international federation of gynecology and obstetrics (FIGO) stage, cell differentiation, and lymph node metastasis. Knockdown of TUG1 expression in cervical cancer cells inhibited cell proliferation and promoted cell apoptosis. Knockdown of TUG1 expression inhibited migration and invasion of cervical cancer cells via the mechanism of epithelial–mesenchymal transition (EMT).