Skip to main content
Figure 2 | Molecular Cancer

Figure 2

From: The role of CCL21/CCR7 chemokine axis in breast cancer-induced lymphangiogenesis

Figure 2

CCR7 activation by CCL21 regulates VEGF-C secretion via the PI3K/AKT signaling pathway. (A) Western blot time course analysis of AKT and ERK1/2 activation in MDA-MB-231 cells following treatment with CCL21 for a total of 60 minutes. Phosphorylation of AKT at Ser 473 and ERK1/2 is observed over the entire duration of stimulation compared to control, untreated cells. (B) Densitometric analysis revealed that phosphorylation of both pathways is significantly induced after 5 min of CCL21 treatment. (C) Western blot and (D) Densitometric analysis indicating that CCL21-induced phosphorylation is dependent on CCR7 activation. Western blot demonstrating that PI3K/AKT inhibitors LY 294002 (E) Akt-1/2 (F), and ERK1/2 inhibitor U0126 (G) can block CCL21/CCR7-mediated phosphorylation in an inhibitor dose-dependent manner. For all experiments, total AKT and total ERK1/2 confirmed the equivalent loading of lanes. (H-J) PI3K/AKT but not ERK1/2 specific inhibitors significantly block CCL21 mediated VEGF-C secretion measured with ELISA. Data are represented as means ± SD (n = 3). Different superscripts indicate statistically significant differences (p < 0.05).

Back to article page