Background
Glioma is one of the most widely diagnosed malignancies worldwide. It has been reported that long noncoding RNAs (lncRNAs) are participators in the tumorgenesis of cancers. Nevertheless, the role and function of lncRNA SNHG17 among glioma is unclear.
Conclusions
The findings that YY1-induced SNHG17 facilitated the glioma progression through targeting miR-506-3p/CTNNB1 axis to activate Wnt/β-catenin signaling pathway offered a brand-new prospects to molecular-targeted treatment for glioma.
Methods
RT-qPCR revealed SNHG17, YY1, miR-506-3p, CTNNB1 expression among glioma cells. CCK-8, colony formation, EdU, flow cytometry, TUNEL and western blot assays revealed the function of SNHG17 in glioma. RIP uncovered SNHG17, miR-506-3p and CTNNB1 enrichment in RISC complex. Luciferase reporter assays and RNA pull down revealed interaction of miR-506-3p with SNHG17 and CTNNB1.
Results
SNHG17 expression was up-regulated in glioma tissues and cells. SNHG17 silence attenuated cell proliferation and promoted apoptosis and repressed tumor growth. Moreover, SNHG17 was up-regulated by transcription factor YY1. Mechanistically, SNHG17 activated Wnt/β-catenin signaling pathway in glioma. CTNNB1 was referred to as the mRNA of β-catenin, we validated that SNHG17 bound to miR-506-3p to induce CTNNB1 and activate Wnt/β-catenin signaling pathway. Rescue experiments indicated that CTNNB1 overexpression abolished the inhibitory effects of SNHG7 inhibition on glioma progression. Conclusions: The findings that YY1-induced SNHG17 facilitated the glioma progression through targeting miR-506-3p/CTNNB1 axis to activate Wnt/β-catenin signaling pathway offered a brand-new prospects to molecular-targeted treatment for glioma.