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Fig. 3 | Cancer Cell International

Fig. 3

From: Long noncoding RNA SNHG17 induced by YY1 facilitates the glioma progression through targeting miR-506-3p/CTNNB1 axis to activate Wnt/β-catenin signaling pathway

Fig. 3

SNHG17 activated Wnt/β-catenin signaling pathway in glioma. a CCK-8 assay demonstrated that by adding the activator of Wnt/β-catenin signaling pathway (LiCl), the suppressed function of SNHG17 depletion on cell proliferation was rescued. Jagged1 and CD40L were added to rescue the effects of SNHG17 knockdown as well. b, c Colony formation and EdU assay manifested that the cell proliferation ability repressed by SNHG17 silence was only recovered by adding LiCl rather than Jagged1 and CD40L. d, e Flow cytometry and TUNEL assays manifested that cell apoptosis induced by SNHG17 down-regulation was abolished by adding LiCl rather than Jagged1 and CD40L. f Western blot assay uncovered the protein level of cleaved-caspase3, cleaved-caspase9 and Bax. g TOP/FOP flash assay showed the luciferase activity of TOP and FOP vectors. hj CCK-8, colony formation and EdU assays unveiled that cell proliferation was blocked by adding the inhibitor of Wnt/β-catenin signaling pathway. k, l Flow cytometry and TUNEL assays demonstrated that cell apoptosis was enhanced via adding the inhibitor of Wnt/β-catenin signaling pathway. m The protein level of cleaved-caspase3, cleaved-caspase9 and Bax was elevated in western blot assay. *P < 0.05, **P < 0.01

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