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. 2016 Dec 27;8(6):9922–9934. doi: 10.18632/oncotarget.14266

Figure 4. IL-17A inhibits autophagy by activating STAT3.

Figure 4

A. The representative images of Western blots and the summary ratio of p-STAT3 to STAT3 in hepatic tissues. B and C. IL-17A stimulated the concentration-and time-dependent phosphorylation of STAT3 in AML-12 cells. The AML-12 cells were treated with the indicated concentrations of IL-17A for 24 hours or the cells were treated with 30 ng ml-1 of IL-17A for the indicated times, and the level of p-STAT3 and STAT3 was detected with Western blot assay. D. AML-12 cells were starved for 2 hours and treated with or without the indicated concentrations of IL-17A or STATTIC. The summary ratio of p-STAT3 to STAT3 was detected with Western blotting. E. Confocal analysis of LC3 expression in AML-12 cells. (F-G) STATTIC protected IL-17A (30 ng ml-1) from the inhibition of the starvation-induced autophagy in AML-12 cells. The expression of autophagy-associated proteins was detected with Western blotting. H. Silencing STAT3 prevented IL-17A-suppersed autophagy. STAT3 gene in AML-12 cells were silenced by STAT3 siRNA or vector and starved for 2 hours and treated with or without the indicated concentrations of IL-17A (30 ng ml-1). The aggregation of p62 was detected with confocal microscopy. I-J The expression of p-STAT3, STAT3, soluble-and insoluble-p62 in AML-12 cells was analyzed with Western blotting. Data are mean ± SEM of three independent assays.