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Fig. 4 | Cancer Cell International

Fig. 4

From: BMX-ARHGAP fusion protein maintains the tumorigenicity of gastric cancer stem cells by activating the JAK/STAT3 signaling pathway

Fig. 4

BMX-ARHGAP overexpression induces the activation of JAK/STAT3 signaling pathway by upregulating BMX-SH2. a Protein expression of BMX-ARHGAP and BMX-SH2 in transfected SGC7901 cells measured by western blot assay; b the protein expression of JAK2 and STAT3 and their phosphorylation extents after transfection measured by western blot assay; c the extent of STAT3 phosphorylation in the nucleus and cytoplasm measured by western blot assay; C cytoplasm, N nucleus, D protein expression of CD133, CD44, SOX2 and Nanog in transfected SGC7901 cells determined by western blot assay; *p < 0.05 vs. the cells transfected with pcDNA3.1 or treated with pcDNA3.1-BMX-ARHGAP and PBS. Measurement data were expressed as mean ± standard deviation; data in a were analyzed by independent t test and those in b–d were analyzed by one-way analysis of variance; each experiment was repeated three times. BMX bone marrow kinase on chromosome X, ARHGAP RhoA GTPase activating protein, SH2 Src homology region 2, PBS phosphate buffer saline, JAK2 Janus kinase 2, STAT3 signal transducer and activator of transcription 3

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