Figure 4
From: The FGFR4-388arg Variant Promotes Lung Cancer Progression by N-Cadherin Induction
N-cadherin is involved in the pro-oncogenic role of Arg388 FGFR4 overexpression. (A) N-cadherin silencing in the FGFR4-388Arg-overexpressing H2009 cell line using a shRNA approach. Clonability (B) and soft agar assays (C) of the FGFR4-388Arg-overexpressing, N-cadherin silenced H2009 cell line. (D) Relative tumor growth of the xenograft in immunodeprived nude mice of these cell lines. (E) Western blot showing the STAT3 activation suspension by the STAT3 inhibitor SI3-201 along the time, which is accompanied by N-cadherin protein levels reduction, in the FGFR4-388Arg-overexpressing H2009 and H226 cell lines. SI3-201 exposure in hours is indicated in the figure. (F) Western blot showing the effect of STAT3 inhibition and N-cadherin shRNA silencing in several cancer-related downstream signaling pathways in the EV, FGFR4-388Gly and -388Arg-overexpressing H2009 cell line. In soft agar and clonability assays, colony number representation is shown. All values were normalized to empty vector control for each replicate of the experiment and the mean and standard deviation of every normalized replicate are represented. For western blots, a representative blot is shown. EV = Empty Vector control, FGFR4-Gly = FGFR4-388Gly overexpressing, FGFR4-Arg = FGFR4-388Arg overexpressing. p-Values are represented as asterisks (*p < 0,05; **p < 0,01; ***p < 0,001). EV1 = Empty Vector 1, EV2 = Empty vector 2, FGFR4-Gly = FGFR4-388Gly overexpressing, FGFR4-Arg = FGFR4-388 FGFR4 overexpressing, shN1-cad = N-cadherin shRNA 1 silenced, shN2-cad = N-cadherin shRNA 2 silenced.
