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. 2018 Aug 16;51(10):e6839. doi: 10.1590/1414-431X20186839

Figure 6. BMI1 inhibited the apoptotic pathway and activated the Notch and mTOR pathways. Protein expression was determined by western blotting. A and B, BMI1 was abnormally expressed after cell transfection. C and D, Bcl-2 expression was down-regulated while expressions of p16, cleaved caspase-9, and cleaved caspase-3 were up-regulated by BMI1 silence. E and F, Phosphorylated levels of key kinases in the Notch and mTOR pathways were increased by BMI1 overexpression. BMI1: B-lymphoma Mo-MLV insertion region 1; pEX-BMI1: recombined overexpression vector of BMI1; shBMI1: pENTRTM/U6 vector carrying small hairpin RNA targeting BMI1; shNC: pENTRTM/U6 vector carrying a non-targeting sequence; p16: multiple tumor suppressor 1; Bcl-2: B-cell lymphoma 2; mTOR: mammalian target of rapamycin; p70S6K: p70 ribosomal protein S6 kinase; p-: phosphorylated.

Figure 6.