1. Academic Validation
  2. Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration

Upregulation of long noncoding RNA TUG1 promotes cervical cancer cell proliferation and migration

  • Cancer Med. 2017 Feb;6(2):471-482. doi: 10.1002/cam4.994.
Yingying Hu 1 Xiangwei Sun 2 Chenchen Mao 2 Gangqiang Guo 3 Sisi Ye 3 Jianfeng Xu 2 Ruanmin Zou 4 Jun Chen 3 Ledan Wang 1 Ping Duan 1 Xiangyang Xue 3
Affiliations

Affiliations

  • 1 Department of Obstetrics and Gynecology, Second Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
  • 2 Department of General Surgery, First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
  • 3 Department of Microbiology and Immunology, Institute of Molecular Virology and Immunology, Institute of Tropical Medicine, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
  • 4 Department of Obstetrics and Gynecology, First Affiliated Hospital, Wenzhou Medical University, Wenzhou, Zhejiang, 325000, China.
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.

Keywords

Bcl-2; LncRNA; TUG1; cervical cancer; epithelial-mesenchymal transition.

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