| Literature DB >> 27998761 |
Dong Liu1, Yawei Li1, Gang Luo2, Xingyuan Xiao1, Dan Tao3, Xinchao Wu4, Miao Wang1, Chao Huang1, Liang Wang1, Fuqing Zeng5, Guosong Jiang6.
Abstract
Emerging evidences have indicated that long non-coding RNAs (LncRNAs) play vital roles in cancer development and progression. Previous studies have suggested that overexpression of SPRY4-IT1 predicates poor prognosis and promotes tumor progress in several cancers. However, the underlying mechanism of SPRY4-IT1 in bladder cancer remains unknown. In this study, we found that SPRY4-IT1 knockdown induced inhibition of cell proliferation, cell migration and invasion ability, and caused promotion of apoptosis in bladder cancer both in vitro and in vivo. Mechanistically, knockdown of SPRY4-IT1 increased the expression of miR-101-3p and subsequently inhibited the expression of EZH2 at posttranscriptional level. Importantly, SPRY4-IT1 could directly interact with miR-101-3p and down-regulation of miR-101-3p efficiently reversed the suppression of EZH2 induced by SPRY4-IT1 shRNA. Thus, SPRY4-IT1 positively regulated the expression of EZH2 through sponging miR-101-3p, and played an oncogenic role in bladder cancer progression. Together, our study elucidates the role of LncRNA SPRY4-IT1 as a miRNA sponge in bladder cancer, and sheds new light on LncRNA-directed diagnostics and therapeutics in bladder cancer.Entities:
Keywords: Bladder cancer; EZH2; Long noncoding RNA; SPRY4-IT1; miR-101-3p
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Year: 2016 PMID: 27998761 DOI: 10.1016/j.canlet.2016.12.005
Source DB: PubMed Journal: Cancer Lett ISSN: 0304-3835 Impact factor: 8.679