Fig. 1.

Expression of MET and VEGFR2 in epithelial cancer cells and suppression of VEGFR2 by HGF–MET signaling.

(A) Immunohistochemical (IHC) analysis of MET and VEGFR2 expression in an example of primary NSCLC adenocarcinoma.

(B) Summary of VEGFR2 expression as determined by IHC in NSCLC patient tumor samples.

(C) Expression of MET and VEGFR2 mRNAs in patient-derived lung tumor samples xenografted in mice.

(D) Expression levels of MET (blue) and VEGFR2 (red) mRNA (a.u., arbitrary units) in cancer cell lines based on microarray analysis data.

(E) Immunoblot analysis of VEGFR2, MET and phospho-MET (pMET) in cell lines that display high mRNA levels of MET and VEGFR2.

(F) H441 cells were treated with Dox to induce shRNA-based MET knockdown (shMET) or with 1 μM MET SMI (GDC-0712) for 48 h and analyzed by immunoblot.

(G) Cells were treated with HGF (100 ng/ml) for 15 min or 24 h in the absence (all) or presence (PC3) of METi (GDC-0712, 1 μM) and levels of VEGFR2, pMET and MET were analyzed by immunoblot.

(H) Cells were treated as in F and amounts of VEGFR2, pMET and MET were analyzed by immunoblot.