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Figure 2 | BMC Cancer

Figure 2

From: Transcriptional activation of the Axl and PDGFR-α by c-Met through a ras- and Src-independent mechanism in human bladder cancer

Figure 2

Expression of c-Met, phosphorylated c-Met, Axl and PDGFR-α in NIH/3T3 and NIH-Met5 cells in the presence or absence of tetracycline. A: A 192 RTK gene cDNA chip was used to screen the gene expression profiles which are positively correlated with c-Met in NIH/3T3 and inducible NIH-Met5 cell lines. A total of 8 RTK genes were shown to positively correlate with c-Met over-expression by CAST analysis (Methods). Only the gene expression profiles of c-Met, Axl and PDGFR-α are shown. NIH/3T3 (1D): the parental NIH/3T3 cell without Tet for 24 h; NIH-Met5 (1D): NIH-Met5 cell without Tet for 24 h; 4D: NIH-Met5 cell with Tet for 24 h followed by Tet-free treatment for another 4 days; 7D: NIH-Met5 cell with Tet for 24 h followed by Tet-free treatment for another 7 days. Relative expression level of each gene is obtained as compared with the common reference RNA [47] B: The expression levels of c-Met, p-Met, Axl and PDGFR-α were evaluated in NIH/3T3 and NIH-Met5 cells without Tet treatment (lanes 1 and 3), or after treatment for 24 h first and then replaced with Tet-free medium for additional 4 and 7 days, (lanes 4 and 5) by Western blotting. β-actin was used as an internal control. The numbers under each band represent the relative intensity.

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