Fig. 6: Wnt3a promotes transient p-ERK via EGFR deactivation while EGF promotes sustained p-ERK in E/M cells. | British Journal of Cancer

Fig. 6: Wnt3a promotes transient p-ERK via EGFR deactivation while EGF promotes sustained p-ERK in E/M cells.

From: Wnt/ERK/CDK4/6 activation in the partial EMT state coordinates mammary cancer stemness with self-renewal and inhibition of differentiation

Fig. 6

a IB of p-ERK, p-EGFR (Y1173), p-EGFR (T669), ERK, EGFR in E/M cells stimulated with 100 ng/ml Wnt3a/1%FBS/RPMI at the indicated time points. b IB of p-ERK, ERK, p-EGFR (Y1173), p-EGFR (T669), EGFR, in E/M cells treated with vehicle or 1 μM PD901 for 24 h, followed by 100 ng/ml Wnt3a in 1%FBS/RPMI for 0.5 h. c IB of p-ERK, p-EGFR (Y1173), FOXC2, ERK, EGFR in E/M cells stimulated with 100 ng/ml Wnt3a or EGF in 0.2%FBS/RPMI at indicated time points. d IF for CD104 (red) and CD44 (green) in E/M cells stimulated with 100 ng/ml Wnt3a or EGF for 4 h in 0.2%FBS/RPMI; 20 μm. e IF for EGFR (FITC) in E/M cells (top panels) treated with vehicle or 1 μM PD901 (MEKi) for 24 h, followed by 100 ng/ml Wnt3a in 0.2%FBS/RPMI for 0.5 h; 20 μm. f EGFR immunostaining (TRITC) in E/M tumours that were treated with vehicle (left panel) as compared to Abemaciclib (CDK4/6i) plus PD901 (MEKi) in vivo (middle and right panel).

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