Long non-coding RNA UBE2CP3 promotes tumor metastasis by inducing epithelial-mesenchymal transition in hepatocellular carcinoma

// Shun-Wang Cao 1 , Jin-Lan Huang 2 , Jing Chen 1 , Yan-Wei Hu 1 , Xiu-Mei Hu 1 , Ting-Yu Ren 3 , Shi-Hao Zheng 4 , Jin-Duan Lin 1 , Jing Tang 5 , Lei Zheng 1 and Qian Wang 1 1 Laboratory Medicine Center, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China 2 Department of Clinical Laboratory, First Affiliated Hospital of Fujian Medical University, Fuzhou, Fujian, China 3 Department of Clinical Laboratory Medicine Center, Shenzhen Hospital of Southern Medical University, Shenzhen, Guangdong, China 4 Department of Neurosurgery, Fujian Provincial Hospital, Fuzhou, Fujian, China 5 Guangdong Provincial Key Laboratory of Gastroenterology, Department of Gastroenterology, Nanfang Hospital, Southern Medical University, Guangzhou, Guangdong, China Correspondence to: Qian Wang, email: nfyywangqian@163.com Lei Zheng, email: nfyyzl@163.com Keywords: long non-coding RNA, UBE2CP3, HCC, metastasis, EMT Received: February 13, 2017      Accepted: June 02, 2017      Published: June 16, 2017 ABSTRACT Hepatocellular carcinoma (HCC) is a highly aggressive, solid malignancy that has a poor prognosis. Long non-coding RNAs (lncRNAs) have been found to be dysregulated in various cancers, including HCC. However, the molecular mechanism involving lncRNAs in HCC remains largely unknown. In this study, lncRNAs differentially expressed between HCC and corresponding non-cancerous tissue were identified by microarray analysis. A specific differentially expressed lncRNA UBE2CP3 (ubiquitin conjugating enzyme E2 C pseudogene 3) was identified. LncRNA UBE2CP3 was frequently up-regulated in HCC samples as assessed by quantitative real-time polymerase chain reaction (qRT-PCR) and in situ hybridization (ISH) experiments. Clinical data showed that high levels of lncRNA UBE2CP3 were correlated with poor prognosis in HCC patients. Functional studies demonstrated that over-expression of lncRNA UBE2CP3 promoted cell invasion and migration in vitro and in vivo . Mechanistically, enhanced expression of lncRNA UBE2CP3 increased the expression of Snail1 and N-cadherin, but decreased the expression of E-cadherin, thus promoting the process of epithelial to mesenchymal transition (EMT) and finally inducing cell invasion and migration. Furthermore, serum levels of lncRNA UBE2CP3 were increased in HCC patients and decreased after surgery. Our results suggest that lncRNA UBE2CP3 promotes the metastasis of HCC and that serum lncRNA UBE2CP3 may be a new biomarker for the diagnosis of HCC.