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. 2019 Nov 13;7(1):1901728. doi: 10.1002/advs.201901728

Figure 3.

Figure 3

IL1R2 regulated BMI1 protein stability. A) RNA‐seq analysis results showed that target genes of BMI1 signaling and TNFα signaling were enriched in SUM159‐IL1R2 and SUM159‐icd‐IL1R2 cells. B) Overexpression of IL1R2 or icd‐IL1R2 promoted BMI1 protein expression. C–E) Silencing of BMI1 reversed the enrichment of the BTIC population, cell proliferation and migration induced by IL1R2 overexpression in SUM159 cells (*, p < 0.05; **, p < 0.01 vs the group indicated). F) IL1R2 protein interacted with BMI1 in the Co‐IP assay. G,H) icd‐IL1R2 and BMI1 were colocalized in cell nucleus of SUM159 cells. I,J) Silencing of IL1R2 promoted BMI1 protein degradation in SUM149 and SUM159 cells under CHX treatment. BMI1 expression measured semiquantitatively with ImageJ software (http://rsb.info.nih.gov/ij/index.html). Relative protein levels were determined by densitometry and calculated as the ratio of the interest protein to its loading control, fold of change was shown. K) Overexpression of IL1R2 or icd‐IL1R2 inhibited ubiquitination of BMI1 in SUM159 cells.