Figure 3. Tumorigenic effects of IL-17 are associated with Stat3 activation and up-regulation of oncogenic genes. B16 tumors were harvested from WT, IL-17−/−, IFN-γ−/−, and IFN-γ−/−IL-17−/− mice 20 d after tumor challenge. (A and B) Stat3 activation in B16 tumors in vivo is notably diminished by IL-17 ablation. (A) Frozen tumor sections were stained with antibodies specific to phospho-Stat3 (pStat3; green). Results are representative of three independent experiments. Bar, 100 µm. (B) Western blot analysis of phospho-Stat3, total Stat3, and β-actin in protein extracts prepared from freshly harvested B16 tumors (representative of three experiments). (C and D) IL-17 deletion inhibits expression of Stat3-downstream oncogenic genes. Western blot analysis of tumor protein extracts to detect Bcl-xL, Bcl-2, vascular endothelial growth factor, MMP9, and β-actin protein levels (representative of two independent experiments).
Figure 3.

Tumorigenic effects of IL-17 are associated with Stat3 activation and up-regulation of oncogenic genes. B16 tumors were harvested from WT, IL-17−/−, IFN-γ−/−, and IFN-γ−/−IL-17−/− mice 20 d after tumor challenge. (A and B) Stat3 activation in B16 tumors in vivo is notably diminished by IL-17 ablation. (A) Frozen tumor sections were stained with antibodies specific to phospho-Stat3 (pStat3; green). Results are representative of three independent experiments. Bar, 100 µm. (B) Western blot analysis of phospho-Stat3, total Stat3, and β-actin in protein extracts prepared from freshly harvested B16 tumors (representative of three experiments). (C and D) IL-17 deletion inhibits expression of Stat3-downstream oncogenic genes. Western blot analysis of tumor protein extracts to detect Bcl-xL, Bcl-2, vascular endothelial growth factor, MMP9, and β-actin protein levels (representative of two independent experiments).

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