The Epithelial-to-Mesenchymal Transition in Breast Cancer: Focus on Basal-Like Carcinomas

被引:114
作者
Fedele, Monica [1 ]
Cerchia, Laura [1 ]
Chiappetta, Gennaro [2 ]
机构
[1] Inst Expt Endocrinol & Oncol, CNR, I-80131 Naples, Italy
[2] Fdn G Pascale, IRCCS, Dipartimento Ric Traslaz & Supporto Percorsi Onco, SC Genom Funz,Ist Nazl Tumori, I-80131 Naples, Italy
关键词
breast cancer; TNBC; EMT; tumor plasticity; molecular signaling; exosomes; miRNAs; v3; differentiation therapy; RECEPTOR TYROSINE KINASES; TGF-BETA; STEM-CELLS; PLASMINOGEN-ACTIVATOR; SIGNALING-PATHWAY; TUMOR-CELLS; METASTASIS; CATENIN; NOTCH; EMT;
D O I
10.3390/cancers9100134
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
Breast cancer is a heterogeneous disease that is characterized by a high grade of cell plasticity arising from the contribution of a diverse range of factors. When combined, these factors allow a cancer cell to transition from an epithelial to a mesenchymal state through a process of dedifferentiation that confers stem-like features, including chemoresistance, as well as the capacity to migrate and invade. Understanding the complex events that lead to the acquisition of a mesenchymal phenotype will therefore help to design new therapies against metastatic breast cancer. Here, we recapitulate the main endogenous molecular signals involved in this process, and their cross-talk with paracrine factors. These signals and cross-talk include the extracellular matrix; the secretome of cancer-associated fibroblasts, macrophages, cancer stem cells, and cancer cells; and exosomes with their cargo of miRNAs. Finally, we highlight some of the more promising therapeutic perspectives based on counteracting the epithelial-to-mesenchymal transition in breast cancer cells.
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页数:19
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