Journal
ONCOTARGET
Volume 8, Issue 67, Pages 110785-110796Publisher
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.22720
Keywords
miR-19; RUNX3; beta-catenin; TCF4; glioma
Categories
Funding
- National High Technology Research [81101915, 30872985, 81301018]
- China National Natural Scientific Fund [81101915, 30872985, 81301018]
- China Scholarship Council (CSC)
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Accumulating data demonstrates t hat the network dysregulation of microRNA-medicated target genes is involved in glioma. We have previously found miR-19a/b overexpression in glioma cell lines and specimens with various tumour grades. However, there was no report on the function and regulatory mechanism of miR-19a/b in glioma. In this study, based on our previous research data, we first determine the inverse relationship between miR-19 (miR-19a and miR-19b) and RUNX3 which is also identified the reduced expression in tumour tissues by real-time PCR and IHC. Luciferase reporter assay and western blot analysis revealed that RUNX3 was a direct target of miR-19. Down-regulation of miR-19 dramatically inhibited proliferation, invasion and induced the cell cycle G1 arrest and apoptosis, at least partly via the up-regulation of RUNX3. Furthermore, Mechanistic investigation indicated that knockdown of miR-19 repressed the beta-catenin/TCF4 transcription activity. In conclusion, our study validates a pathogenetic role of miR-19 in glioma and establishes a potentially regulatory and signaling involving miR-19 /RUNX3/beta-catenin, also suggesting miR-19 may be a candidate therapeutic target in glioma.
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