Figure 6

Activation Effects of IGF-I on IGF-IR pathway in human uterine leiomyoma cells.

(A,B) Phosphorylated IGF-IRβ was significantly higher 5 min after IGF-I (100ng/mL) treatment and remained increased until 60 min (P < 0.05). Downstream adapter protein IRS-1 followed the same pattern (P < 0.05). Phosphorylation of another adapter protein Shc (P < 0.05) and downstream effector protein AKT (P < 0.05) and MAPKp44/42 (P < 0.05) were significantly increased at 5 min and peaked at 10 min when the cells were treated with IGF-I, then fell back to basal levels at 60 min. (C) The activation of IGF-IRβ, Shc, and MAPKp44/42 induced by IGF-I was neutralized partially (Shc: about 40% and MAPKp44/42: about 80%, P < 0.05) when the cells were incubated with anti-IGF-IRB antibody before IGF-I treatment. However, the induction of phosphorylated IRS-I at 10′, 30′, and 60′, and phosphorylated AKT at 5′, 10′, 30′ and 60′, were not significantly decreased. The western blot analysis was done at least three times in three independent in vitro experiments with comparable results. The phospho/total ratio data was expressed as means ± SE of three replicates.