MiRNA-125a-5p inhibits glioblastoma cell proliferation and promotes cell differentiation by targeting TAZ

•Expression of miR-125a-5p is inversely correlated with that of TAZ in glioma cells.•MiR-125a-5p represses TAZ expression in glioma cells.•MiR-125a-5p directly targets the 3′ UTR of TAZ mRNA and promotes its degradation.•MiR-125a-5p represses CTGF and survivin via TAZ, and inhibits glioma cell growt...

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Veröffentlicht in:Biochemical and biophysical research communications 2015-02, Vol.457 (2), p.171-176
Hauptverfasser: Yuan, Jian, Xiao, Gelei, Peng, Gang, Liu, Dingyang, Wang, Zeyou, Liao, Yiwei, Liu, Qing, Wu, Minghua, Yuan, Xianrui
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Sprache:eng
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Zusammenfassung:•Expression of miR-125a-5p is inversely correlated with that of TAZ in glioma cells.•MiR-125a-5p represses TAZ expression in glioma cells.•MiR-125a-5p directly targets the 3′ UTR of TAZ mRNA and promotes its degradation.•MiR-125a-5p represses CTGF and survivin via TAZ, and inhibits glioma cell growth.•MiR-125a-5p inhibits the stem cell features of HFU-251 MG cells. Glioblastoma (GBM) is the most lethal brain tumor due to the resistance to conventional therapies, such as radiotherapy and chemotherapy. TAZ, an important mediator of the Hippo pathway, was found to be up-regulated in diverse cancers, including in GBM, and plays important roles in tumor initiation and progression. However, little is known about the regulation of TAZ expression in tumors. In this study, we found that miR-125a-5p is an important regulator of TAZ in glioma cells by directly targeting the TAZ 3′ UTR. MiR-125a-5p levels are inversely correlated with that of TAZ in normal astrocytes and a panel of glioma cell lines. MiR-125a-5p represses the expression of TAZ target genes, including CTGF and survivin, and inhibits cell proliferation and induces the differentiation of GBM cells; whereas over-expression of TAZ rescues the effects of miR-125a-5p. This study revealed a mechanism for TAZ deregulation in glioma cells, and also demonstrated a tumor suppressor role of miR-125a-5p in glioblastoma cells.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2014.12.078