LncRNA RSU1P2 contributes to tumorigenesis by acting as a ceRNA against let-7a in cervical cancer cells

Qian Liu, Xu Guo, Shengshun Que, Xi Yang, Hongxia Fan, Min Liu, Xin Li, Hua Tang

Oncotarget · 2016 · 85 citations · 33 references

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// Qian Liu 1, * , Xu Guo 1, * , Shengshun Que 1, * , Xi Yang 1 , Hongxia Fan 1 , Min Liu 1 , Xin Li 1 and Hua Tang 1 1 Tianjin Life Science Research Center, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China * These authors have contributed equally to this work Correspondence to: Hua Tang, email: htang2002@yahoo.com Keywords: ceRNA, miRNA, Let-7, N-myc, lnc-RNA Received: December 13, 2015     Accepted: June 17, 2016     Published: July 26, 2016 ABSTRACT Long non-coding RNAs (lncRNAs) can regulate gene expression at different levels and are widely participate in various physiological and pathological processes. Emerging evidences suggests that a number of differentially expressed lncRNAs are involved in tumorigenesis. However, the function and expression regulation of a vast majority of these unique RNAs is little known. Here, we found that the lncRNA Ras suppressor protein 1 pseudogene 2 (RSU1P2) is upregulateded in cervical cancer tissues and has a tumour-promoting role. We revealed that RSU1P2 acts as a competitive endogenous RNA (ceRNA) through regulating the expression of IGF1R, N-myc and EphA4. The mechanism of this regulation is via competition for the shared microRNA let-7a. This competition promotes the malignant phenotype of cervical carcinoma cells. The transcription factor N-myc forms a positive feedback loop with RSU1P2 by in turn activating its expression, thereby enhancing its oncogenic capacity. Hence, cancer-selective targeting of RSU1P2 could have strong benefits.

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