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. 2014 Mar 4;44(5):1433–1442. doi: 10.3892/ijo.2014.2319

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Copyright © 2014, Spandidos Publications

This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.

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Figure 7. — Effect of wortmannin, PD98059, cytochalasin B and Rho inhibitor. The amount of cell adhesion of H-ALCL cells was inhibited by wortmannin treatment (^*P=0.02; ^**P=0.002) (A). The amount of cell invasive capacity was inhibited by treatment of PD98059 and wortmannin (^*P=0.01; s^**P=0.0069) (B). The amount of cell adhesion of H-ALCL cells was enhanced by cytochalasin B treatment (^*P=0.029) (C). The amount of cell invasion to galectin-1 was dramatically inhibited by treatment of cytochalasin B (^*P=0.028) (D). The amount of cell invasion to galectin-1 was dramatically inhibited by Rho inhibitor, C3 transferase treatment (^*P=0.006) (E). The data are representative of at least two independent experiments in triplicate.

Figure 7. — Effect of wortmannin, PD98059, cytochalasin B and Rho inhibitor. The amount of cell adhesion of H-ALCL cells was inhibited by wortmannin treatment (^*P=0.02; ^**P=0.002) (A). The amount of cell invasive capacity was inhibited by treatment of PD98059 and wortmannin (^*P=0.01; s^**P=0.0069) (B). The amount of cell adhesion of H-ALCL cells was enhanced by cytochalasin B treatment (^*P=0.029) (C). The amount of cell invasion to galectin-1 was dramatically inhibited by treatment of cytochalasin B (^*P=0.028) (D). The amount of cell invasion to galectin-1 was dramatically inhibited by Rho inhibitor, C3 transferase treatment (^*P=0.006) (E). The data are representative of at least two independent experiments in triplicate.