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. 2003 Sep;163(3):1001–1011. doi: 10.1016/s0002-9440(10)63460-8

Figure 2.

Figure 2.

A: Autocrine IGF-IR activation in parental L3.6pl pancreatic cancer cells. Cells were grown for 48 hours and medium was either replaced with fresh 10% FBS-MEM (lane 1) 8 hours before harvesting the cells (control), or remained unchanged for 48 hours (conditioned medium) (lane 2). Cell lysates were subjected to Western blot analysis of IGF-IR phosphorylation. Equal loading was verified by probing for β-actin. When cells are allowed to grow in their own conditioned medium, the IGF-IR is phosphorylated. In contrast, when the medium is changed to prevent the cells from conditioning their own medium, there is no receptor phosphorylation. B: Effect of IGF-IR inhibition on constitutive and inducible activation of signaling pathways. IGF-IR DN- and pcDNA-transfected L3.6pl cells were treated for the indicated times with rhIGF-I (100 ng/ml) under serum-reduced conditions (1% FBS-MEM). Protein extracts were examined by Western blot analysis for IGF-IR phosphorylation and activated signaling pathways. Equal loading was verified by probing for β-actin. No differences in Akt phosphorylation were observed among transfected cell lines. P38 and JNK phosphorylation levels were not affected by rhIGF-I (not shown).