Interleukin-6 Mediates Epithelial–Stromal Interactions and Promotes Gastric Tumorigenesis
Figure 3
Interleukin-6 (IL-6) promoted gastric tumor development through STAT3 activation.
(A) Immunoblot analysis of phosphorylated and total STAT3 in non-tumor tissues and tumors from wild-type (WT) and IL-6−/− mice in the N-methyl-N-nitrosourea (MNU)-induced gastric tumorigenesis model. (B) Immunohistochemical analysis of phosphorylated STAT3 in WT (left) and IL-6−/− (right) mice in the MNU-induced gastric tumorigenesis model. (C) Immunohistochemical analysis of phosphorylated STAT3 in Helicobacter pylori–negative healthy control, Helicobacter pylori–positive gastritis, gastric adenoma, and gastric cancer (original magnification, ×200). (D) Immunoblot analysis of phosphorylated and total STAT3 in SH101 and AGS cells treated with pyridone 6 (P6; 1 µM) for the indicated times. (E) SH101 and AGS cells were cultured with or without P6 (1 µM), and cell numbers were determined at the indicated times. Data are plotted as means (± standard deviations). *P<0.05 compared with cells without P6. (F) qRT-PCR for the indicated genes in gastric cancer cell line NUGC4 when co-cultured with fibroblasts with or without neutralizing anti-IL-6 receptor antibody (MRA). *P<0.05 compared with co-culture without MRA. (G) Immunohistochemical analysis of CD44 in stomach tissues of WT and IL-6−/− mice in chemically-induced gastric tumorigenesis model. (original magnification, ×200).