Skip to main content
Figure 8 | Breast Cancer Research

Figure 8

From: Autocrine WNT signaling contributes to breast cancer cell proliferation via the canonical WNT pathway and EGFR transactivation

Figure 8

Schematic representation of wingless and integration site growth factor (WNT)-induced epidermal growth factor receptor (EGFR) transactivation. Our results show that Wnt1 induces a signaling cascade that links the activation of EGFR in a manner dependent on Dishevelled, SRC, metalloprotease, and EGF-like ligand to the sFRP1-sensitive activation of Frizzled receptors. The activation of EGFR, which may occur via phosphorylation of Y845, an SRC phosphorylation site, triggers activation of the extracellular signal-regulated kinase 1/2 (ERK1/2) pathway. Together with the canonical WNT/β-catenin pathway and its target genes, including c-Myc, the ERK1/2 pathway promotes proliferation and survival of breast cancer cells. Furthermore, activation of the ERK1/2 signaling by Wnt1 may contribute to the development of anti-estrogen resistance. DVL, Dishevelled; EGF, epidermal growth factor; ER, estrogen receptor; sFRP1, secreted Frizzled-related protein 1.

Back to article page