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. 2020 Jan 10;14(2):309–328. doi: 10.1002/1878-0261.12622

Figure 7.

Figure 7

DANCR sufficiently stimulated inflammation and targeted SOCS3 expression through EZH2‐mediated epigenetic regulation in normal breast epithelial cells or breast cancer cells of low malignancy. ELISA assay showed that DANCR overexpression potently stimulated the secretions of IL‐6 (A) and TGF‐β (B) into the conditioned medium of indicated cells. RT‐qPCR revealed increased expressions of IL‐6 (C) and TGF‐β (D) in DANCR cells. (E,F) Western blot showed that DANCR markedly promoted the activation of p65 and STAT3, but reduced the expression of SOCS3 in indicated cells. (G,H) Western blot on EZH2, H3K27me3, H3, and Hsp60 revealed specific increases of H3K27me3 in DANCR cells. ChIP assay showed that the binding of EZH2 (I) and H3K27me3 (J) to the promoter of SOCS3 was significantly increased in DANCR cells. (K) RNA immunoprecipitation assay revealed the specific interaction between DANCR and EZH2 in MCF‐10A and MCF‐7. IgG was used as the negative control. n = 3, data are shown as mean ± SD. Student’s t‐test (A–F) and one‐way ANOVA (G–K) were used to determine statistical significance: *P < 0.05, **P < 0.01, ***P < 0.001.