| Literature DB >> 24931370 |
Zhiyong Yan1, Jianpeng Wang1, Chao Wang1, Yingbing Jiao1, Weiguo Qi1, Shusheng Che2.
Abstract
We found that miR-96 is overexpressed in glioma, and its level inversely correlates with the survival of patients. The reduction in miR-96 abundance suppresses the proliferation and colony formation of glioma cells. The tumorigenicity of U-87 MG cells is reduced by miR-96 silencing. miR-96 contributes to the activation of Wnt/β-catenin pathway in glioma cells. HMG-box transcription factor 1 (HBP-1), a Wnt/β-catenin pathway inhibitor, is suppressed by miR-96. The reactivation of Wnt/β-catenin signaling causes an increase in the proliferation of glioma cells, and a decrease in miR-96 expression. On the other hand, HBP1 silencing promotes miR-96 expression. Collectively, miR-96 contributes to the progression of glioma by enhancing the activation of the Wnt/β-catenin pathway, and the miR-96/HBP1/Wnt/β-catenin regulatory circuitry promotes the proliferation of glioma cells.Entities:
Keywords: Glioma; HMG-box transcription factor 1; Proliferation; Wnt/β-catenin; miR-96
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Year: 2014 PMID: 24931370 DOI: 10.1016/j.febslet.2014.06.017
Source DB: PubMed Journal: FEBS Lett ISSN: 0014-5793 Impact factor: 4.124