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. 2016 Jun 21;7(30):48180–48192. doi: 10.18632/oncotarget.10193

Figure 7. Low-dose ICJ targets non-canonical signaling of TGF-beta.

Figure 7

A. Co-immunoprecipitation analysis in MDA-231 cells. Cells were pre-treated with ICJ for 36 hours and stimulated by TGF-beta for 15 minutes. IP: Immunoprecipitation; IB: Immunoblotting; Lysates: Whole cell lysate control. B. Western blot analysis of FAK phosphorylation in ICJ treated MDA-231 and 4T1 cells for 36 hours. C. Detection of Src phosphorylation in ICJ treated and TGF-beta stimulated MDA-231 and 4T1 cells. D, E. Detection of the phosphorylation of MAPK members in ICJ treated breast cancer cells for 36 hours. F. Time-course detection of p-38 phosphorylation level in response to ICJ and TGF co-treatment. The p38 phosphorylation was monitored from 0.5 to 36 hours after treatment in 4T1 cells. Result revealed that ICJ could inhibit p38 pathway in a wide time-window. G. Detection of the ITGB3 expression in primary tumor samples from experiment mentioned in Figure 3. Four mice samples were randomly selected in each group (named M1 to M4). H. Detection of ITGB3 expression in TGF-beta and ICJ combined treated MDA-231 cells for 36 hours. I. In vitro analysis of ITGB1 and ITGB3 expression in MDA-231 cells.