Long non-coding RNA TUG1 is up-regulated in hepatocellular carcinoma and promotes cell growth and apoptosis by epigenetically silencing of KLF2

Molecular Cancer

Research

Ming Sun¹  Fu-Zhen Qi²  Ming-De Huang³  Tong-Peng Xu⁴  Pei Ma⁴  Yong-qian Shu⁴  Wen-Ming Chen⁵ 

[1] Department of Biochemistry and Molecular Biology, Nanjing Medical University, Nanjing City, Jiangsu Province, People’s Republic of China;Department of Hepatopancreatobiliary Surgery, Huai’an First People’s Hospital, Nanjing Medical University, 223300, Huai’an City, Jiangsu Province, People’s Republic of China;Department of Medical Oncology, Huai’an First People’s Hospital, Nanjing Medical University, 223301, Huai’an City, Jiangsu Province, People’s Republic of China;Department of Oncology, First Affiliated Hospital, Nanjing Medical University, Nanjing City, Jiangsu Province, People’s Republic of China;Department of Oncology, Jining No.1 People’s Hospital, No.6, Jiankang Road, 272011, Jining City, Shandong Province, People’s Republic of China;

关键词: Long non-coding RNA;    TUG1;    HCC;    Proliferation;    KLF2;   

DOI  :  10.1186/s12943-015-0431-0

 received in 2015-03-11, accepted in 2015-08-11,  发布年份 2015

来源: Springer

【 摘 要 】

BackgroundHepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide, and the biology of this cancer remains poorly understood. Recent evidence indicates that long non-coding RNAs (lncRNAs) are found to be dysregulated in a variety of cancers, including HCC. Taurine Up-regulated Gene 1 (TUG1), a 7.1-kb lncRNA, recruiting and binding to polycomb repressive complex 2 (PRC2), is found to be disregulated in non-small cell lung carcinoma (NSCLC) and esophageal squamous cell carcinoma (ESCC). However, its clinical significance and potential role in HCC remain unclear.Methods and resultsIn this study, expression of TUG1 was analyzed in 77 HCC tissues and matched normal tissues by using quantitative polymerase chain reaction (qPCR). TUG1 expression was up-regulated in HCC tissues and the higher expression of TUG1 was significantly correlated with tumor size and Barcelona Clinic Liver Cancer (BCLC) stage. Moreover, silencing of TUG1 expression inhibited HCC cell proliferation, colony formation, tumorigenicity and induced apoptosis in HCC cell lines. We also found that TUG1 overexpression was induced by nuclear transcription factor SP1 and TUG1 could epigeneticly repress Kruppel-like factor 2 (KLF2) transcription in HCC cells by binding with PRC2 and recruiting it to KLF2 promoter region.ConclusionOur results suggest that lncRNA TUG1, as a growth regulator, may serve as a new diagnostic biomarker and therapy target for HCC.

【 授权许可】

CC BY   
© Huang et al. 2015