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. 2017 Apr 27;8(24):38113–38135. doi: 10.18632/oncotarget.17494

Figure 4. Inhibition of IL-4R blocks IL-4-induced NOX1 expression.

Figure 4

A.-B. Knockdown of IL-4Rα blocks NOX1 expression at the mRNA A. and protein B. levels. HT-29 cells were transiently transfected with either of the two different IL-4Rα specific siRNAs and treated with IL-4 (50 ng/ml) 24 h later. Cells were harvested 24 h post-treatment and examined by quantitative RT-PCR A. or by Western analysis B.. β-actin and GAPDH served as the internal controls for RT-PCR or Western analysis, respectively. C. IL-4-induced NOX1 expression requires the presence of IL-4R. IL-4-induced NOX1 expression was abolished in HT-29 by the concurrent presence of an IL-4Rα neutralizing antibody in the absence of FBS, as shown by quantitative RT-PCR. D. IL-4 stimulates cell proliferation through the involvement of IL-4R. IL-4Rα antibody (1 ng/ml) significantly inhibited IL-4-enhanced HT-29 proliferation. Data represent the mean ± SD of three experiments. ** = P < 0.01; *** = P < 0.001.