期刊
CNS NEUROSCIENCE & THERAPEUTICS
卷 18, 期 9, 页码 722-728出版社
WILEY
DOI: 10.1111/j.1755-5949.2012.00349.x
关键词
Glioblastoma; hTERT; miR-21; STAT3
资金
- China National Natural Scientific Fund [81101901, 81172389, 81072078]
- National High Technology Research and Development Program 863 [2012AA02A508]
Background and purpose As an important oncogenic miRNA, miR-21 has been reported to play crucial roles in glioblastoma (GBM) carcinogenesis. However, the precise biological function and molecular mechanism of miR-21 in GBM remain elusive. This study is designed to explore the mechanism of miR-21 involved in the control of GBM cell growth. Methods and results MTT assay, cell cycle analysis, and apoptosis analysis showed that reduction of miR-21 inhibited cell growth in U87 and LN229 GBM cells. Further, reduction of miR-21 decreased the expression of human telomerase reverse transcriptase (hTERT) and repressed STAT3 expression and STAT3 phosphorylation. STAT3 inhibition led to a remarkable depletion of hTERT at both mRNA and protein levels by binding to the hTERT gene promoter by performing luciferase reporter assay and chromatin Immunoprecipitation PCR. Finally, knockdown of miR-21 considerably inhibited tumor growth and diminished the expression of STAT3 and hTERT in xenograft model. Conclusion Our findings indicate that miR-21 regulates hTERT expression mediated by STAT3, therefore controlling GBM cell growth.
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