Skip to main content
. 2012 Sep 28;24(2):343–349. doi: 10.1093/annonc/mds463

Figure 3.

Figure 3

Western blotting for c-Met, phosphorylated c-Met and selected downstream mediators in renal cell carcinoma (RCC) cell lines. (A) c-Met and phosphorylated c-Met (Y1234/Y1235 kinase and Y1349 carboxy-terminal docking site domains) were present in all cell lines with varying expression levels without supplemental HGF stimulation. (B and C) A498 and 769P cell lines were treated with increasing concentrations of SU11274 or ARQ 197 for 24 h. Total c-Met expression remained relatively stable with drug treatment. Phosphorylated c-Met expression was highest in control (untreated cells) and was blocked with increasing concentrations of SU11274 or ARQ 197. Downstream changes in the c-Met pathway were seen predominantly in phosphorylated AKT, while decreased phosphorylated ERK1/2 and phosphorylated rpS6 (P70S6Kinase) occurred at higher c-Met inhibitor concentrations.