Fig. 6.
Fig. 6. IGF-I–induced proliferation and the PI-3K pathway. / IGF-I–induced proliferation is predominantly associated with the PI-3K pathway. H929 cells were starved for 2 hours in serum-free growth media followed by treatment with the PI-3K inhibitor LY294002 (10 μM), the MAPK inhibitor PD98059 (50 μM), or the p70S6 kinase inhibitor rapamycin (10 nM). Cells were then seeded at 3 × 104 per well in 96-well plates in serum-free media with or without 100 ng/mL IGF-I for 24, 48, or 72 hours. Proliferation was measured by MTT assay (panel A). DNA synthesis was also measured by [3H]-thymidine uptake at 48 hours following treatment as above (panel B). Results are presented as mean ± SE (n = 4). Data are representative of 3 separate experiments. *P < .01 versus control. **P < .001 versus control.

IGF-I–induced proliferation and the PI-3K pathway.

IGF-I–induced proliferation is predominantly associated with the PI-3K pathway. H929 cells were starved for 2 hours in serum-free growth media followed by treatment with the PI-3K inhibitor LY294002 (10 μM), the MAPK inhibitor PD98059 (50 μM), or the p70S6 kinase inhibitor rapamycin (10 nM). Cells were then seeded at 3 × 104 per well in 96-well plates in serum-free media with or without 100 ng/mL IGF-I for 24, 48, or 72 hours. Proliferation was measured by MTT assay (panel A). DNA synthesis was also measured by [3H]-thymidine uptake at 48 hours following treatment as above (panel B). Results are presented as mean ± SE (n = 4). Data are representative of 3 separate experiments. *P < .01 versus control. **P < .001 versus control.

Close Modal

or Create an Account

Close Modal
Close Modal