Figure 6
Figure 6. Effects of stimulation by IGF-I and specific blockade of IGF-IR on ALK+ ALCL cells. To confirm the findings of inhibition of IGF-IR signaling by PPP in ALK+ ALCL cells and to rule out that these findings were due to nonspecific effects, 3 specific approaches were used that involved stimulating the cells with IGF-I for 24 hours after growing the cells in serum-free RPMI medium for 3 hours. (A) Stimulation of IGF-IR signaling by IGF-I promotes serum-deprived ALK+ ALCL cell migration, which is abrogated by treating the cells with anti–IGF-I neutralizing antibody or anti–IGF-IR blocking antibody. The results are representative of 2 consistent experiments. (B) Stimulation of IGF-IR signaling by IGF-I induces a concentration-dependent increase in the viability of serum-deprived ALK+ ALCL and P6 (positive control) cells. This effect was also reversed when specific antibodies were used to neutralize IGF-I or to block IGF-IR. The results are representative of 2 consistent experiments. (C) The increase in cell viability could be due to a decrease in the apoptosis of serum-deprived ALK+ ALCL cells. Treating the cells with either anti–IGF-I neutralizing antibody or anti–IGF-IR blocking antibody similarly reversed this effect of IGF-I. The results are representative of 2 consistent experiments.

Effects of stimulation by IGF-I and specific blockade of IGF-IR on ALK+ ALCL cells. To confirm the findings of inhibition of IGF-IR signaling by PPP in ALK+ ALCL cells and to rule out that these findings were due to nonspecific effects, 3 specific approaches were used that involved stimulating the cells with IGF-I for 24 hours after growing the cells in serum-free RPMI medium for 3 hours. (A) Stimulation of IGF-IR signaling by IGF-I promotes serum-deprived ALK+ ALCL cell migration, which is abrogated by treating the cells with anti–IGF-I neutralizing antibody or anti–IGF-IR blocking antibody. The results are representative of 2 consistent experiments. (B) Stimulation of IGF-IR signaling by IGF-I induces a concentration-dependent increase in the viability of serum-deprived ALK+ ALCL and P6 (positive control) cells. This effect was also reversed when specific antibodies were used to neutralize IGF-I or to block IGF-IR. The results are representative of 2 consistent experiments. (C) The increase in cell viability could be due to a decrease in the apoptosis of serum-deprived ALK+ ALCL cells. Treating the cells with either anti–IGF-I neutralizing antibody or anti–IGF-IR blocking antibody similarly reversed this effect of IGF-I. The results are representative of 2 consistent experiments.

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