Skip to main content
. 2012 Nov;14(11):1015–1022. doi: 10.1593/neo.12870

Figure 3.

Figure 3

RPTP-β regulates HGF-induced Grb2 binding to Met and downstream activation of MEK and ERK in HNSCC cells. (A) UMSCC-22B metastatic HNSCC tumor cells were infected with empty adenovirus or RPTP-β-expressing adenovirus. Forty-eight hours post-infection, cells were treated with vehicle (-, Ctrl) or HGF (10 ng/ml, +) for 15 minutes. Met was immunoprecipitated from whole-cell lysates, and immunoprecipitates were analyzed for Grb2 and Met by Western blot. (B and C) UMSCC-22B cells were treated as in A, except HGF treatment time was 30 minutes, and analyzed for MEK phosphorylation (B) and ERK phosphorylation (C). (D and E) UMSCC-22A primary HNSCC tumor cells were infected with NT or RPTP-β-targeting shRNA lentivirus. UMSCC-22A cells were treated as in A, except HGF treatment time was 30 minutes, and analyzed for MEK phosphorylation (D) and ERK phosphorylation (E). Immunoreactive bands were quantified by chemifluorescence using a STORM Image Analyzer. Data are means ± SEM, N = 3; *P < .05. Insets show representative Western blots.