Skip to main content
. 2016 Aug 12;7(38):61107–61120. doi: 10.18632/oncotarget.11243

Figure 6. Inhibition of signaling pathways identifies key mediators of the IL-6-driven decrease in p53 in a cell-specific manner.

Figure 6

(A) In HCT-116 cells, treatment with p-Stat3 inhibitor BP-1-102 at 5 ug/mL abrogates the down-regulation of p53 by IL-6 as well as the increase in MDM2. Successful inhibition of PI3K, as observed via lack of phosphorylation of effector AKT, using 20 uM LY294002 abrogates IL-6-downregulation of p53 as well as the increase in MDM2. Inhibition of MEK, as observed via lack of phosphorylation of effector molecules ERK 1/2, with 20 uM U0126 has no effect on IL-6-driven regulation of p53 or MDM2, as expected. β-actin was used as a loading control. (B) Treatment of HT-1080 with BP-1-102 abrogates the down-regulation of p53 by IL-6 as well as the increase in MDM2. Neither treatment with LY294002 or U0126 in these cell lines upsets the effects of IL-6 on MDM2 levels, as expected. U0126 does not affect IL-6 downregulation of p53. However, due to the effects of LY294002 on blocking nuclear transport of MDM2 the p53 levels do not decrease in response to IL-6 in this condition. β-actin was used as a loading control.