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Figure 8. The effects of hypoxia and PTK787 combined with hypoxia on tumor and endothelial cell migration. A, in the tumor cell line, hypoxia inhibited the motility of tumor cells through the membrane, and the suppression was further enhanced by the administration of PTK787. The expression of Rac1, Rho, and <t>P-Akt</t> was reduced with hypoxia alone and the combined approach. B, in the endothelial cell line, hypoxia enhanced the motility of endothelial cells across the membrane, whereas adminis- tration of PTK787 could reverse the hypoxia-enhanced migration. Hypoxia up-regulated the expression of Rac1, but it was reduced by the administration of PTK787. The expression of Rho was decreased with the hypoxic stimulation, and the down-regulation was further enhanced by the administration of PTK787. Hypoxia had no obvious effect on the expression of P-Akt, but the combined treatment significantly down- regulated the expression of P-Akt. Representative of four independent experiments. *, P < 0.05, compared with NT under normoxia; #, <0.05, compared with NT under hypoxia. NT, sham operation (no treatment).
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Figure 8. The effects of hypoxia and PTK787 combined with hypoxia on tumor and endothelial cell migration. A, in the tumor cell line, hypoxia inhibited the motility of tumor cells through the membrane, and the suppression was further enhanced by the administration of PTK787. The expression of Rac1, Rho, and <t>P-Akt</t> was reduced with hypoxia alone and the combined approach. B, in the endothelial cell line, hypoxia enhanced the motility of endothelial cells across the membrane, whereas adminis- tration of PTK787 could reverse the hypoxia-enhanced migration. Hypoxia up-regulated the expression of Rac1, but it was reduced by the administration of PTK787. The expression of Rho was decreased with the hypoxic stimulation, and the down-regulation was further enhanced by the administration of PTK787. Hypoxia had no obvious effect on the expression of P-Akt, but the combined treatment significantly down- regulated the expression of P-Akt. Representative of four independent experiments. *, P < 0.05, compared with NT under normoxia; #, <0.05, compared with NT under hypoxia. NT, sham operation (no treatment).
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Image Search Results


Journal: PLoS ONE

Article Title: Interferon-γ Suppresses Intestinal Epithelial Aquaporin-1 Expression via Janus Kinase and STAT3 Activation

doi: 10.1371/journal.pone.0118713

Figure Lengend Snippet:

Article Snippet: Phosphorylated AKT (Cat# AF887, R & D Systems, Minneapolis, MN) , 5% BSA in TTBS , 1:400 , goat anti-rabbit.

Techniques: Blocking Assay, Concentration Assay

Figure 8. The effects of hypoxia and PTK787 combined with hypoxia on tumor and endothelial cell migration. A, in the tumor cell line, hypoxia inhibited the motility of tumor cells through the membrane, and the suppression was further enhanced by the administration of PTK787. The expression of Rac1, Rho, and P-Akt was reduced with hypoxia alone and the combined approach. B, in the endothelial cell line, hypoxia enhanced the motility of endothelial cells across the membrane, whereas adminis- tration of PTK787 could reverse the hypoxia-enhanced migration. Hypoxia up-regulated the expression of Rac1, but it was reduced by the administration of PTK787. The expression of Rho was decreased with the hypoxic stimulation, and the down-regulation was further enhanced by the administration of PTK787. Hypoxia had no obvious effect on the expression of P-Akt, but the combined treatment significantly down- regulated the expression of P-Akt. Representative of four independent experiments. *, P < 0.05, compared with NT under normoxia; #, <0.05, compared with NT under hypoxia. NT, sham operation (no treatment).

Journal: Molecular Cancer Therapeutics

Article Title: High doses of tyrosine kinase inhibitor PTK787 enhance the efficacy of ischemic hypoxia for the treatment of hepatocellular carcinoma: dual effects on cancer cell and angiogenesis

doi: 10.1158/1535-7163.mct-06-0149

Figure Lengend Snippet: Figure 8. The effects of hypoxia and PTK787 combined with hypoxia on tumor and endothelial cell migration. A, in the tumor cell line, hypoxia inhibited the motility of tumor cells through the membrane, and the suppression was further enhanced by the administration of PTK787. The expression of Rac1, Rho, and P-Akt was reduced with hypoxia alone and the combined approach. B, in the endothelial cell line, hypoxia enhanced the motility of endothelial cells across the membrane, whereas adminis- tration of PTK787 could reverse the hypoxia-enhanced migration. Hypoxia up-regulated the expression of Rac1, but it was reduced by the administration of PTK787. The expression of Rho was decreased with the hypoxic stimulation, and the down-regulation was further enhanced by the administration of PTK787. Hypoxia had no obvious effect on the expression of P-Akt, but the combined treatment significantly down- regulated the expression of P-Akt. Representative of four independent experiments. *, P < 0.05, compared with NT under normoxia; #, <0.05, compared with NT under hypoxia. NT, sham operation (no treatment).

Article Snippet: The protein levels of caspase-9, Bcl-2, cyclin D1, phosphorylated Akt (P-Akt; mouse anti-rat caspase-9, Bcl-2, cyclin D1, and P-Akt monoclonal antibodies, Cell Signaling Technology, Inc., Beverly, MA), Rac1 and Rho (mouse anti-rat Rac1 and Rho monoclonal antibodies, BD Biosciences PharMingen), VEGF (mouse anti-rat VEGF monoclonal antibody, R&D Systems, Minneapolis, MN), and Flt-1 and Flk-1 (rabbit anti-rat Flt-1 and Flk-1 polyclonal antibodies, Santa Cruz Biotechnology, Santa Cruz, CA) were detected by standard Western blot protocol using 12% SDS-PAGE gel.

Techniques: Migration, Membrane, Expressing