期刊
CELL ADHESION & MIGRATION
卷 9, 期 3, 页码 233-246出版社
TAYLOR & FRANCIS INC
DOI: 10.4161/19336918.2014.983794
关键词
epithelial-mesenchymal transition; signal transduction; transforming growth factor; tumor invasiveness; bHLH; basic helix-loop-helix; BMP; bone morphogenetic protein; CSC; cancer stem cell; DNMT; DNA methyltransferase; EMT; epithelial-mesenchymal transition; FGF; fibroblast growth factor; HDAC; histone deacetylase; lncRNA; long non-coding RNA; mTORC; mammalian target of rapamycin complex; MET; mesenchymal-epithelial transition; miRNA; micro-RNA; MAPK; mitogen activated protein kinase; PDGF; platelet derived growth factor; PRC; polycomb repressive complex; TF; transcription factor; TGF; transforming growth factor
类别
资金
- Ludwig Institute for Cancer Research
- Swedish Cancer Society
- Swedish Research Council
- Marie Curie Initial Training Network ITLiver under the European Union FP7 program
Epithelial-mesenchymal transition (EMT) refers to plastic changes in epithelial tissue architecture. Breast cancer stromal cells provide secreted molecules, such as transforming growth factor (TGF), that promote EMT on tumor cells to facilitate breast cancer cell invasion, stemness and metastasis. TGF signaling is considered to be abnormal in the context of cancer development; however, TGF acting on breast cancer EMT resembles physiological signaling during embryonic development, when EMT generates or patterns new tissues. Interestingly, while EMT promotes metastatic fate, successful metastatic colonization seems to require the inverse process of mesenchymal-epithelial transition (MET). EMT and MET are interconnected in a time-dependent and tissue context-dependent manner and are coordinated by TGF, other extracellular proteins, intracellular signaling cascades, non-coding RNAs and chromatin-based molecular alterations. Research on breast cancer EMT/MET aims at delivering biomolecules that can be used diagnostically in cancer pathology and possibly provide ideas for how to improve breast cancer therapy.
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