Signaling Crosstalks: EGFR and TAZ in Breast Cancer

Abstract

Breast cancer is driven by multiple molecular aberrations, transforming benign epithelial cells into metastatic cancer. Identification of key signaling nodes underlying metastasis and resistance to treatment is crucial to improving targeted therapies. This review examines two oncogenes driving epithelial to mesenchymal transition (EMT) and the acquisition of cancer stem cell properties. The epidermal growth factor receptor (EGFR), a well-established oncogene driving migration, survival, and proliferation, activates several downstream signaling cascades including the AKT and MAPK pathways. EGFR overexpression, mutation, and mislocalization are frequently observed in breast cancer. TAZ, transcriptional coactivator with PDZ-binding motif, induces and sustains EMT and is required for the acquisition of breast cancer stem cell traits. The emerging crosstalk between these pathways yields insights into early mammary tumorigenesis, epithelial plasticity, and the metastatic niche, suggesting novel avenues for the development of targeted therapies.