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Fig. 3 | Journal of Experimental & Clinical Cancer Research

Fig. 3

From: Intrinsic fluorescence of the clinically approved multikinase inhibitor nintedanib reveals lysosomal sequestration as resistance mechanism in FGFR-driven lung cancer

Fig. 3

Fluorescence-based monitoring of ABCB1-mediated reduction of intracellular nintedanib levels. a Expression of ABCB1 in DMS114 cells and their isogenic nintedanib-resistant counterpart DMS114/NIN was analyzed by Western blot. ß-actin served as loading control. b Impact of ABCB1 inhibition by elacridar on the cytotoxic activity of nintedanib in DMS114 cells and their resistant subline was analyzed by MTT assay 72 h after drug exposure. *** p < 0.001, 2-way ANOVA, Tukey’s post-test. c Impact of 10 μM elacridar on the intracellular accumulation of 10 μM nintedanib in DMS114 and DMS114/NIN cells was analyzed by confocal fluorescence microscopy after 1 h drug exposure. The scale bar indicates 10 μm. d Quantification of relative fluorescence intensities of micrographs shown in (c) is plotted normalized to nintedanib-treated DMS114 control cells. *** p < 0.001, 2-way ANOVA, Tukey’s post-test. e Impact of 10 μM elacridar on the intracellular accumulation of 10 μM nintedanib in DMS114 and DMS114/NIN cells was measured at the indicated time-points by flow cytometry using the FITC channel. *** p < 0.001, 2-way ANOVA, Tukey’s post-test. ns non-significant

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