Figure 7
Antibody inhibition of PAR2 but not PAR1 cleavage attenuated human breast cancer growth. (A) MDA-MD 231mfp cells were injected subcutaneously with 1 mg of rabbit anti-PAR2 polyclonal antibody, preimmune rabbit IgG, anti-PAR1 monoclonal antibody ATAP2 or murine IgG1 control (TIB115). A composite of 2 independent experiments is shown. Tumor volumes of anti-PAR2-treated groups were significantly different from all other groups by ANOVA, followed by Kruskal- Wallis, P < .001. (B) Inhibition of tumor growth in the absence of Fc-mediated killing is demonstrated by injecting tumor cells in the presence of 1 mg of anti-PAR2 Fab′2 fragment. The preparation of these experiments inhibited TF-VIIa-mediated activation of human PAR2 by more than 95%, but mouse PAR2 only marginally (<50%). Final tumor volumes were different at P < .05, t test.

Antibody inhibition of PAR2 but not PAR1 cleavage attenuated human breast cancer growth. (A) MDA-MD 231mfp cells were injected subcutaneously with 1 mg of rabbit anti-PAR2 polyclonal antibody, preimmune rabbit IgG, anti-PAR1 monoclonal antibody ATAP2 or murine IgG1 control (TIB115). A composite of 2 independent experiments is shown. Tumor volumes of anti-PAR2-treated groups were significantly different from all other groups by ANOVA, followed by Kruskal- Wallis, P < .001. (B) Inhibition of tumor growth in the absence of Fc-mediated killing is demonstrated by injecting tumor cells in the presence of 1 mg of anti-PAR2 Fab′2 fragment. The preparation of these experiments inhibited TF-VIIa-mediated activation of human PAR2 by more than 95%, but mouse PAR2 only marginally (<50%). Final tumor volumes were different at P < .05, t test.

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