CREB up-regulates long non-coding RNA, HULC expression through interaction with microRNA-372 in liver cancer

Jiayi Wang(Ruijin Hospital), Xiangfan Liu(Shanghai Jiao Tong University), Huacheng Wu(Shanghai Jiao Tong University), Peihua Ni(Shanghai Jiao Tong University), Zhidong Gu(Shanghai Jiao Tong University), Yongxia Qiao(Shanghai Jiao Tong University), Ning Chen(Shanghai Jiao Tong University), Fenyong Sun(Shanghai Jiao Tong University), Qishi Fan(Shanghai Jiao Tong University)
Nucleic Acids Research
April 27, 2010
Cited by 1,007Open Access
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Abstract

Long non-coding RNA (lncRNA), highly up-regulated in liver cancer (HULC) plays an important role in tumorigenesis. Depletion of HULC resulted in a significant deregulation of several genes involved in liver cancer. Although up-regulation of HULC expression in hepatocellular carcinoma has been reported, the molecular mechanisms remain unknown. In this study, we used in vivo and in vitro approaches to characterize cancer-dependent alterations in the chromatin organization and find a CREB binding site (encompassing from -67 to -53 nt) in the core promoter. Besides, we also provided evidence that PKA pathway may involved in up-regulation of HULC. Furthermore, we demonstrated HULC may act as an endogenous 'sponge', which down-regulates a series of microRNAs (miRNAs) activities, including miR-372. Inhibition of miR-372 leads to reducing translational repression of its target gene, PRKACB, which in turn induces phosphorylation of CREB. Over-expression of miR-372 decreases the association of CREB with the proximal promoter, followed by the dissociation of P300, resulting in a change of the histone 'code', such as in deacetylation and methylation. The study elucidates that fine tuning of HULC expression is part of an auto-regulatory loop in which it's inhibitory to expression and activity of miR-372 allows lncRNA up-regulated expression in liver cancer.


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