Notch promotes breast cancer progression through tumor initiating cell maintenance, tumor cell fate specification, proliferation, survival, and motility. In addition, Notch is recognized as a decisive mechanism in regulating various juxtacrine and paracrine communications in the tumor microenvironment (TME). In this chapter, we review recent studies on stress-mediated Notch activation within the TME and sequelae such as angiogenesis, extracellular matrix remodeling, changes in the innate and adaptive immunophenotype, and therapeutic perspectives.
Keywords: Angiogenesis; Basal-like; Breast cancer; CCL2; CD8+ T-cell; Cancer-associated fibroblast; Cellular stress; DLL; Extracellular matrix; IL1β; Immune checkpoint blockade; Immunophenotype; JAG; Notch; PD-1; RBPJҡ; TGF-β; TRB3; Triple negative; Tumor microenvironment; Tumor-associated macrophage; USP9x; Urokinase-type plasminogen activator; γ-secretase.