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. Author manuscript; available in PMC: 2011 Feb 9.
Published in final edited form as: Cancer Res. 2009 Feb 3;69(4):1284–1292. doi: 10.1158/0008-5472.CAN-08-2331

Figure 6.

Figure 6

Combined inhibition of EGFR and HH/GLI efficiently reduces mouse BCC cell growth in vitro. A, immunohistochemical analysis of EGFR expression in a human nodular BCC. B, total EGFR and activated EGFR (p-EGFR) expression in mouse BCC cell lines; the respective genotype (and irradiation) of the cell lines is indicated below. C, single or combined treatment of CSZ1 cells with 5 μmol/L gefitinib (gef) and 10 μmol/L GANT61 (left), 10 μmol/L GANT61, and 10 μmol/L U0126 (right), or 5 μmol/L cyclopamine (cyc) and JUN shRNA (bottom left). Statistical analysis was done by Student's t test. **, P < 0.005. Data represent the mean value of three independent experiments. D, model of integration of EGFR and HH/GLI signaling in the regulation of GLI/EGF target genes and oncogenic transformation. In addition to activation of JUN/AP-1, stimulation of MEK/ERK may also promote the nuclear import of GLIact, thereby enhancing the synergistic effect (46). cyc, cyclopamine; gef, gefitinib; e, epidermis; t, tumor.