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. Author manuscript; available in PMC: 2010 Mar 27.
Published in final edited form as: Oncogene. 2007 Mar 19;26(38):5577–5586. doi: 10.1038/sj.onc.1210348

Figure 4.

Figure 4

NRP1 promotes survival of U87MG cells by enhancing autocrine HGF/SF/c-Met signaling. (A) Overexpression of NRP1 promotes U87MG cell survival. Data of cell survival assays are shown as mean±s.d. (B) Inhibition of HGF/SF, but not FGF-2 or VEGF, suppresses NRP1-promoted U87MG cell survival. Data of cell survival assays are shown as mean±s.d. (C) Inhibition of tumor cell-derived HGF/SF, but not VEGF or FGF-2, suppresses NRP1-potentiated activation of c-Met and Bad. IP and IB analyses of various U87MG cells treated with or without the HGF/SF neutralizing antibody. (D) Serum starvation did not alter NRP1 expression in U87MG, LacZ and NRP1 cells. IB analyses of various cell lysates under the same conditions as in (A). (E) and (F) Inhibition of endogenous c-Met but not Sema 3A attenuates NRP1-potentiated U87MG cell viability. (E) Suppression of endogenous c-Met and Sema 3A by siRNA. IB analyses of c-Met and Sema 3A proteins in various U87MG cells. (F) Cell survival assays of siRNA-transfected U87MG and NRP1 cells. Data are shown as mean±s.d. In (B–D), c-Met, Bad and β-actin were used as loading controls. Results in (A–F) are representative of three independent experiments.