Fig. 2: Malignant transformation by patient-specific FGFR2-fusion proteins. | Nature Communications

Fig. 2: Malignant transformation by patient-specific FGFR2-fusion proteins.

From: The molecular interaction pattern of lenvatinib enables inhibition of wild-type or kinase-mutated FGFR2-driven cholangiocarcinoma

Fig. 2

a Proliferation analyses of FGFR2-fusion expressing cell lines using SRB assays after 7 days in culture, ****P ≤ 0.0001 compared to control transduced NIH3T3 cells with one-way ANOVA with Dunnett’s multiple comparison test. Bars represent mean ± SD (n = 30 vials examined over 10 independent experiments). b Quantification of soft agar colony formation after 21 days with FGFR2-fusion-expressing cell lines and a control cell line transfected with the empty vector, ****P ≤ 0.0001 compared to control transfected NIH3T3 cells with one-way ANOVA with Dunetts’s multiple comparison test. Bars represent mean ± SD (n = 8 vials (empty vector, FGFR2-AHCYL2, FGFR2-SH3GLB1), n = 10 vials (FGFR2-BICC)) examined over 3 independent experiments. c Representative images of soft agar assays with the indicated cell lines after 21 days. d Representative Western blot analysis of FGFR2 downstream signals in NIH3T3 cell lines stably transfected with patient-derived FGFR2 gene fusions (FGFR2-BICC1, FGFR2-SH3GLB1, FGFR2-AHCYL2) or control transfected NIH3T3 cells (n = 3 biologically independent samples).

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