Upregulated lncRNA-UCA1 contributes to progression of hepatocellular carcinoma through inhibition of miR-216b and activation of FGFR1/ERK signaling pathway.

摘要: // Feng Wang 1, * , Hou-Qun Ying 2, Bang-Shun He 1 Yu-Qin Pan Qi-Wen Deng Hui-Ling Sun 3 Jie Chen Xian Liu Shu-Kui Central Laboratory, Nanjing First Hospital, Medical University, Nanjing, Jiangsu, China 2 college, Southeast Department of Life Sciences, Normal These authors have contributed equally to this work Correspondence to: Wang, e-mail: shukwangnj@163.com Keywords: hepatocellular carcinoma, lncRNA, UCA1, miR-216b, FGFR1 Received: November 17, 2014      Accepted: January 26, 2015      Published: February 11, 2015 ABSTRACT The long non-coding RNA (lncRNA) urothelial carcinoma-associated (UCA1) has been recently shown be dysregulated, which plays an important role in the progression several cancers. However, biological and clinical significance UCA1 carcinogenesis carcinoma (HCC) remain unclear. Herein, we found that was aberrantly upregulated HCC tissues associated with TNM stage, metastasis postoperative survival. depletion inhibited growth cell lines vitro vivo . Furthermore, could act as endogenous sponge by directly binding miR-216b downregulation expression. In addition, reverse inhibitory effect on cells, might involved derepression fibroblast factor receptor (FGFR1) expression, a target gene activation ERK signaling pathway. Taken together, our data highlights pivotal tumorigenesis HCC. Moreover, present study elucidates novel lncRNA-miRNA-mRNA regulatory network is UCA1-miR-216b-FGFR1-ERK pathway HCC, may help lead better understanding pathogenesis probe feasibility lncRNA-directed diagnosis therapy for deadly disease.