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Fig. 1 | Breast Cancer Research

Fig. 1

From: TNFAIP3 is required for FGFR1 activation-promoted proliferation and tumorigenesis of premalignant DCIS.COM human mammary epithelial cells

Fig. 1

Activation of iFGFR1 induces ERK1/2 activation, cell morphological change, and cell proliferation. a Development of DCIS-Ctrl and DCIS-iFGFR1 cell lines. Cells expanded from single clones were assayed by immunoblotting with HA antibody. DCIS-Ctrl clones had no iFGFR1 expression. Two positive DCIS-iFGFR1 clones (#2 and #6) were detected. b AP20187 treatment had no effect on ERK1/2 in DCIS-Ctrl cell lines #1 and #2, but it increased p-ERK1/2 in DCIS-iFGFR1 cell lines #2 and #6 without affecting total ERK1/2 levels. The relative intensities of p-ERK1/2 to total ERK1/2 bands for each sample were calculated from three independent assays. **** p < 0.0001 by Student’s t test. c AP20187 treatment for the indicated time periods rapidly increased p-ERK1/2 in DCIS-iFGFR1 but not DCIS-Ctrl cells that were pre-cultured in serum-free medium for 12 h. d AP20187 treatment induced a fibroblast-like morphological change of both #2 and #6 DCIS-iFGFR1 cell lines. The upper images were recorded under a phase-contrast microscope. The lower images were recorded from phalloidin-stained cells pretreated with vehicle or AP20187 as indicated. e AP20187 (AP)-treated DCIS-iFGFR1 cells showed lower β-catenin, K8, and E-cadherin and higher vimentin, fibronectin, and N-cadherin when compared with vehicle (V)-treated DCIS-iFGFR1 cells. The relative band intensities shown in the bar graph were obtained from three independent assays. *** and **** p < 0.001 and 0.0001 by Student’s t test. f AP20187-activated iFGFR1 stimulated DCIS-iFGFR1 cell growth. DCIS-Ctrl and DCIS-iFGFR1 cells were treated with vehicle or AP20187 for 1 or 5 days as indicated. Cell viability was assayed from four independent samples by the CellTiter kit. Absorbance was measured at 490 nm. ***p < 0.001 by one-way ANOVA

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