FIGURES 1 and 2:

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FIGURES 1 and 2:

Fig 1: Evidence for c-Met and β1 integrin interaction. (A) Western blot showing robust c-Met and β1 integrin expression in U87MG lysates before and after IP with αV antibody, with c-Met/αV binding doubling at hypoxia relative to normoxia. In SF8244 lysates, (B) c-Met was detected before and after IP with β1 antibody, (C) integrin β1 was detected before and after IP with c-Met antibody, and (D) cMet was detected before and after IP with α5 antibody. (E) PLA of SF8244 on fibronectin revealed areas of α5-c-Met interaction (red dots). Blue=nuclear stain. Scale=20 µm.

Fig 2: Evidence for c-Met and β1 integrin interaction. Amongst intracranial xenografts derived from our previously described bevacizumab-naive U87-IgG R and bevacizumab-resistant U87-Bev xenografts, the latter exhibited areas of β1c-Met interaction after bevacizumab treatment (red dots). Blue=nuclear stain. Scale=20 µm.

FIGURES 3 and 4:

Fig 3: Evidence for c-Met and β1 integrin functional interaction. Increasing fibronectin concentration for 48 hours led to increased cMet phosphorylation.

Fig 4: Targeting β1 integrin or c-Met affects the other in vitro and in vivo. (A) Compared to SF8106 cells transduced with control shRNA, SF8106-shβ1 clones exhibited 50% less c-Met expression by flow cytometry. *P