Figure - PMC

Skip to main content

View full-text article in PMC

. Author manuscript; available in PMC: 2010 Mar 1.

Published in final edited form as: Mol Cancer Res. 2009 Mar 3;7(3):425–432. doi: 10.1158/1541-7786.MCR-08-0342

MDA-MB-231 (A) and SUM-159-PT (B) cells were transfected with either vector control, constitutively active Akt1 (Myr.Akt.HA) along with vector control or mutant GSK-3β (HA.GSK3β.S9A), or mutant GSK-3β alone. 16 h after transfection the ability of the cells to migrate was assessed by a chemomigration assays. A portion of the transfected cells were immunoblotted with anti-HA. (C) SUM-159-PT cells were transfected with either vector control, or mutant GSK-3β (HA.GSK-3β.S9A). Cells were then serum starved for 19 h, then stimulated with IGF-1 for 18 h (100 ng/ml), followed by chemomigration assays. All results are representative of three independent experiments, and were performed in triplicate. Error bars indicate ± SD, with p values as indicated (NS, not significant).

MDA-MB-231 (A) and SUM-159-PT (B) cells were transfected with either vector control, constitutively active Akt1 (Myr.Akt.HA) along with vector control or mutant GSK-3β (HA.GSK3β.S9A), or mutant GSK-3β alone. 16 h after transfection the ability of the cells to migrate was assessed by a chemomigration assays. A portion of the transfected cells were immunoblotted with anti-HA. (C) SUM-159-PT cells were transfected with either vector control, or mutant GSK-3β (HA.GSK-3β.S9A). Cells were then serum starved for 19 h, then stimulated with IGF-1 for 18 h (100 ng/ml), followed by chemomigration assays. All results are representative of three independent experiments, and were performed in triplicate. Error bars indicate ± SD, with p values as indicated (NS, not significant).

HHS Vulnerability Disclosure