Skip to main content
Figure 5 | BMC Cancer

Figure 5

From: GnRH receptor activation competes at a low level with growth signaling in stably transfected human breast cell lines

Figure 5

The level of p-ERK1/2 is influenced by integration of signaling from multiple cell surface receptors, blocking the response to activated GnRH receptor. A. Triptorelin did not affect levels of p-ERK1/2 in serum-starved MCF-7-30 or MDA-MB-231-34 cells. B. Treatment of stably transfected cells with 100 nM Triptorelin transiently elevated levels of phosphorylated ERK1/2 (p-ERK1/2) in serum-starved MCF-7-30-7hygro14 cells but not in the presence of serum. Bar graphs indicate effect of no serum vs with serum on ERK response in MCF7hygro14, statistically significant for no serum, p < 0.05. C. Treatment with IGF-IR inhibitor resulted in rapid and sustained de-phosphorylation of ERK1/2 in MCF-7-30-7hygro14 cells but not in MDA-MB-231-34 cells. D. Rapid re-phosphorylation of ERK1/2 occurred in MCF-7-30-7hygro14 cells when IGF-I receptor inhibitor was washed off and replaced with fresh culture medium but addition of 100 nM Triptorelin did not affect levels of phosphorylated ERK1/2 Re-phosphorylation of ERK1/2 was less marked in HEK293[SCL60] cells and addition of Triptorelin considerably augmented levels of phosphorylated ERK1/2.

Back to article page