Abstract

Abstract BACKGROUND & AIMS: Long noncoding RNAs (lncRNAs) have been identified as novel regulators of biologic behaviors in various cancers. However, the oncogenic mechanisms of lincRNA-UFC1 associated with hepatocellular carcinoma (HCC) growth and progression are still unknown. Here, we delved into the mechanistic aspects of lincRNA-UFC1in HCC progression. METHODS: LncRNA expression profiles are assessed by microarray analysis. Expression of lincRNA-UFC1 was examined in 2 HCC cohorts (cohort 1, n = 49; cohort 2, n = 131) by quantitative real-time PCR or by in situ hybridization. The functions of lincRNA-UFC1 in HCC cells were elucidated by in vitro and in vivo gain- and loss-of-function experiments. The mechanism by which lincRNA-UFC1 contributes to HCC progression was explored through luciferase reporter assays, RNA immunoprecipitation and RNA pull-down assays. RESULTS: LincRNA-UFC1 was strongly upregulated in HCC tissues, compared with corresponding non-tumor tissues in patients from 2 cohorts. LincRNA-UFC1 expression is associated with tumor size, Barcelona Clinic Liver Cancer (BCLC) stage and poor prognosis. Enhanced lincRNA-UFC1 expression promotes cell proliferation and tumor growth, inhibits apoptosis, and induces cell cycle progression, whereas decreased lincRNA-UFC1 expression represented the opposite effects. Furthermore, lincRNA-UFC1 directly interacts with HuR and regulates β-catenin expression. The level of lincRNA-UFC1 is positively correlated with that of β-catenin in HCC tissues. CONCLUSIONS: These findings indicate that lincRNA-UFC1 promotes HCC development and progression, indicating its role as a potential therapeutic target for HCC. Citation Format: LI LIU, Dehua Wu, Chuanhui Cao. lincRNA-UFC1 facilitates cell proliferation and tumor growth in hepatocellular carcinoma by upregulating HuR/β-catenin expression. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 3954. doi:10.1158/1538-7445.AM2015-3954

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