STAT3 and STAT1 mediate IL-11–dependent and inflammation-associated gastric tumorigenesis in gp130 receptor mutant mice
J. Clin. Invest. Matthias Ernst, et al. 118:1727 doi:10.1172/JCI34944 [Go to this article.]

Figure 4
Reduced STAT3 activation and gastric tumor burden in STAT3-ASO–treated gp130^Y757F/Y757F mice. (A) Blood platelet counts of naive adult gp130^Y757F/Y757F mice treated with either vehicle (PBS) or STAT3-ASO at the indicated concentrations every second day over 28 days. Data are expressed as mean ± SD. n = 8 for each treatment group. *P < 0.05 versus vehicle-treated mice. (B) Representative whole-mount appearance of stomachs from mice shown in A. Mice were treated either with vehicle or 50 mg/kg STAT3-ASO. Data points represent the combined wet weight of all excised polyps from individual mice, and the horizontal lines indicate the means. (C and D) Tissue cross-sections of gastric polyps from mice shown in B and stained with either H&E (C) or an antibody against BrdU (D). Scale bars: 100 μm. (E) Immunoblot analyses of antral gastric tissue lysates from individual naive gp130^Y757F/Y757F mice using the indicated antibodies. Mice were treated with PBS, control-ASO, or STAT3-ASO at a final concentration of 50 mg/kg, and each lane represents an individual mouse. (F) Q-PCR analyses of Socs3 and Il11 gene expression in gastric tumors from mice shown in E and treated with either control ASO or STAT3-ASO at 50 mg/kg. Data are expressed as mean ± SD. n = 5 for each treatment group. *P < 0.05.