CXCR4 Antibody - #AF5279

Figure 6 Downregulation of c-Myc enhanced the antitumor effect of bufalin in pancreatic cancer cells through the HIF-1α/SDF-1/CXCR4 pathway. (A) The protein expression of c-Myc, vimentin, E-cadherin, HIF-1α, CXCR4, and SDF-1 in PANC-1 and SW1990 pancreatic cancer cells under different treatments was detected via western blot. (B) Quantification results of protein expressions of c-Myc, vimentin, E-cadherin, HIF-1α, CXCR4, and SDF-1 in PANC-1 pancreatic cancer cells. (C) Quantification results of protein expression of c-Myc, vimentin, E-cadherin, HIF-1α, CXCR4, and SDF-1 in SW1990 pancreatic cancer cells (* p < 0.05, ** p < 0.01 vs control, ▲ p < 0.05, ▲▲ p < 0.01 vs bufalin treatment group, n = 3).

Fig. 5. Dose-response study of quercetin on the migration of PASMCs in vitro. (A) Photographs of the PASMCs migration through the polycarbonate membrane stained by 0.2% crystal violet in hypoxia and treated with increasing concentrations of quercetin for 24 h. (B) Quantification of the number of cells migrating through the polycarbonate membrane of average of 3 independent experiments. (C) Full-length blots of MMP-2, MMP-9, CXCR4, Integrin α1, β1, and α5 and GAPDH are presented. (D) Results were quantified by densitometry analysis of the bands form (C) and then normalization to GAPDH protein. *Po0.05, **Po0.01 compared with control; #Po0.05, ##Po0.01 compared with hypoxia and quercetin treated PASMCs.