The long non-coding RNA CRNDE acts as a ceRNA and promotes glioma malignancy by preventing miR-136-5p-mediated downregulation of Bcl-2 and Wnt2
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Dong-Xue Li1,2, Xiao-Rui Fei2, Yong-Fei Dong2, Chuan-Dong Cheng2, Yang Yang2, Xue-Fei Deng3, Hai-Liang Huang3, Wan-Xiang Niu2, Chen-Xu Zhou2, Cheng-Yu Xia2 and Chao-Shi Niu2
1Shandong University, Jinan, Shandong, China
2Department of Neurosurgery, Anhui Provincial Hospital Affiliated to Anhui Medical University, Hefei, Anhui, China
3School of Basic Medical Sciences, Anhui Medical University, Hefei, Anhui, China
Chao-Shi Niu, email: [email protected]
Keywords: CRNDE, glioma, miR-136-5p, Bcl-2, Wnt2
Received: June 16, 2017 Accepted: September 08, 2017 Published: October 04, 2017
The colorectal neoplasia differentially expressed (CRNDE) gene encodes a long non-coding RNA (lncRNA) that is the most unregulated among 129 lncRNAs differentially expressed in gliomas. In this study, we confirmed high CRNDE expression in clinical glioma specimens and observed through experiments in human glioma cell lines a novel molecular mechanism by which CRNDE may contribute to glioma pathogenesis. By inducing or silencing CRNDE expression, we detected a positive correlation between CRNDE levels and the proliferative, migratory, and invasive capacities of glioma cells, which were concomitant with a decreased apoptosis rate. Our experiments also suggest that these effects are mediated by downregulation of miR-136-5p, which correlated with the glioma WHO grade. Based on predicted CRNDE/miR-136-5p/mRNA interactions, both the mRNA and protein expression analyses suggested that miR-136-5p-mediated repression of Bcl-2 and Wnt2 underlies the pro-tumoral actions of CRNDE. We therefore propose that CRNDE functions as a competing endogenous RNA (ceRNA) that binds to and negatively regulates miR-136-5p, thereby protecting Bcl-2 and Wnt2 from miR-136-5p-mediated inhibition in glioma.
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