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Role of the long non-coding RNA HOTAIR in hepatocellular carcinoma
Liming Wu1,2,3,4, Lele Zhang1,2,3, Shusen Zheng1,2,3
1Collaborative Innovation Center for Diagnosis and Treatment of Infectious Diseases, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang 310003, P.R. China.
Abstract:
A number of recent studies have focused on the association between long non-coding RNAs (lncRNAs) and cancer. HOX transcript antisense RNA (HOTAIR), an lncRNA that functions as a transcriptional modulator, has been implicated in various fundamental biological activities. HOTAIR mediates the trimethylation of histone H3 at lysine 27 and the demethylation of histone H3 dimethyl Lys4 by recruiting the polycomb repressive complex 2 and the lysine-specific demethylase 1/co-repressor of RE1-silencing transcription factor (coREST)/REST complex to the target gene promoters, which leads to gene silencing. Overexpression of HOTAIR in hepatocellular carcinoma (HCC) is strongly associated with an unfavorable prognosis for patients with HCC. HOTAIR promotes the carcinogenic activity of HCC cells through the suppression of RNA binding motif protein 38, triggering the epithelial-mesenchymal transition, and by interacting with microRNAs that act as tumor suppressors. In the present review, the role of the lncRNA HOTAIR in HCC is examined. The potential use of HOTAIR as a biomarker to achieve more accurate prognostic predictions and as an effective therapeutic target for HCC is then discussed.
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