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.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Yan Z,Wang J,Wang C,Jiao Y,Qi W,Che Sdoi
10.1016/j.febslet.2014.06.017subject
Has Abstractpub_date
2014-08-25 00:00:00pages
3038-46issue
17eissn
0014-5793issn
1873-3468pii
S0014-5793(14)00476-1journal_volume
588pub_type
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