Notch Signaling and the Breast Cancer Microenvironment

被引:33
|
作者
Shen, Qiang [1 ]
Reedijk, Michael [1 ]
机构
[1] Univ Hlth Network, Princess Margaret Canc Ctr, Dept Surg Oncol, Toronto, ON, Canada
关键词
Notch; JAG; DLL; gamma-secretase; RBPJ kappa; Breast cancer; Triple negative; Basal-like; Tumor microenvironment; Angiogenesis; Urokinase-type plasminogen activator; Extracellular matrix; TRB3; USP9x; Cellular stress; TGF-beta; IL1; beta; CCL2; Tumor-associated macrophage; CD8+T-cell; Immunophenotype; Cancer-associated fibroblast; PD-1; Immune checkpoint blockade; ENDOTHELIAL GROWTH-FACTOR; EPITHELIAL-MESENCHYMAL TRANSITION; IN-VITRO PROPAGATION; MAMMARY-TUMOR VIRUS; REGULATORY T-CELLS; STROMAL FIBROBLASTS; UBIQUITIN LIGASE; GENE-EXPRESSION; STEM-CELLS; MATRIX METALLOPROTEINASES;
D O I
10.1007/978-3-030-55031-8_12
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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.
引用
收藏
页码:183 / 200
页数:18
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