Fig. 4: SNHG6 epigenetically silenced p27 expression by recruiting EZH2 to its promoter region. | Cell Death Discovery

Fig. 4: SNHG6 epigenetically silenced p27 expression by recruiting EZH2 to its promoter region.

From: Gene amplification-driven lncRNA SNHG6 promotes tumorigenesis via epigenetically suppressing p27 expression and regulating cell cycle in non–small cell lung cancer

Fig. 4

a The relative mRNA expression of cyclin-dependent kinase inhibitors after SNHG6 silencing; b p27 was upregulated after SNHG6 knockdown in protein level; c Overexpression of SNHG6 downregulated the p27 expression in mRNA and protein levels; d SNHG6 had a positive tendency to interact with EZH2 according to catRAPID and the potential binding sites were illustrated; e Knockdown of SNHG6 exerted no influence on the expression of EZH2 in mRNA and protein levels; f RIP assays were employed to verify the interaction between SNHG6 and EZH2 in A549 and SPCA1; g Knockdown of EZH2 upregulated the mRNA and protein expressions of p27 in both cell lines; h SNHG6 upregulation rescued the increased expression of p27 arisen from EZH2 inhibition. i ChIP assays showed that the knockdown of SNHG6 decreased the enrichment of EZH2 and H3K27me3 at the promoter region of p27. The results were from three independent experiments. Data were analyzed by unpaired student’s t-test. ***P < 0.001, **P < 0.01, *P < 0.05. Variables were presented as the mean ± SD.

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