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Fig. 6 | Journal of Experimental & Clinical Cancer Research

Fig. 6

From: Mitochondrial ROS accumulation inhibiting JAK2/STAT3 pathway is a critical modulator of CYT997-induced autophagy and apoptosis in gastric cancer

Fig. 6

CYT997 performs its function through regulation of STAT3 signaling pathway in SGC-7901 and MKN45 cells. a Expression of phosphorylated STAT3(Tyr705) (p-STAT3), phosphorylated JAK2 (p-JAK2) and the major downstream protein Bcl-2, Survivin and Cyclin D1 was detected by western blotting in SGC-7901 and MKN45 cells treated with CYT997. b SGC-7901cells were treated with CYT997 or in combination with IL-6. The expression of p-STAT3 and STAT3 was detected by western blotting in SGC-7901 cells. c-d SGC-7901 cells were treated with CYT997 or in combination with IL-6. The cytoplasmic and nuclear distribution of STAT3 was detected by western blotting c and fluorescent microscope d in SGC-7901 cells. e-h SGC-7901 cells were transfected with STAT3 vector, and then treated with CYT997. The expression of p-STAT3, STAT3, Cyclin D1, Bcl-2 and Survivin was detected by western blotting e. Cell viability was detected by a CCK8 assay f. The cell cycle distribution was analyzed by flow cytometry g. Apoptosis was detected by flow cytometry h. i SGC-7901 cells transfected with STAT3 vector were treated with CYT997. The expression of Cyclin B1, p21, cleaved PARP and cleaved caspase 3 was detected by western blotting. j SGC-7901 cells were treated with CYT997 or in combination with NAC. The expression of p-STAT3, STAT3, p-JAK2, JAK2, Cyclin D1, Bcl-2, and Survivin was detected by western blotting in SGC-7901 cells

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