The relevance of the TGF-β Paradox to EMT-MET programs

Highlights • Mechanisms of the TGF-β Paradox. • EMT:MET cycles in generating cancer initiating cells. • Role of EMT:MET programs in metastatic progression. • EMT programs and the acquisition of chemoresistance. • Mechanisms of oncogenic TGF-β signaling.

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Bibliographische Detailangaben
Veröffentlicht in:	Cancer letters 2013-11, Vol.341 (1), p.30-40
Hauptverfasser:	Morrison, Chevaun D, Parvani, Jenny G, Schiemann, William P
Format:	Artikel
Sprache:	eng
Schlagworte:	aggression Alternative Splicing Animals Bone Morphogenetic Proteins - metabolism carcinogenesis carcinoma Cell Hypoxia cell movement cytotoxicity DNA-Binding Proteins - metabolism Epithelial plasticity Epithelial-Mesenchymal Transition - physiology Fibroblasts - metabolism Fibroblasts - pathology Heat-Shock Proteins - metabolism Hematology, Oncology and Palliative Medicine Humans Integrins - metabolism Metastasis MicroRNAs - genetics MicroRNAs - metabolism Neoplasms - genetics Neoplasms - metabolism Neoplasms - pathology Neoplastic Stem Cells - metabolism Neoplastic Stem Cells - pathology phenotype Proto-Oncogene Proteins c-abl - metabolism relapse Signal Transduction stem cells TGF-β Transcription Factors - metabolism Transforming Growth Factor beta - genetics Transforming Growth Factor beta - metabolism
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Beschreibung
Zusammenfassung:	Highlights • Mechanisms of the TGF-β Paradox. • EMT:MET cycles in generating cancer initiating cells. • Role of EMT:MET programs in metastatic progression. • EMT programs and the acquisition of chemoresistance. • Mechanisms of oncogenic TGF-β signaling.
ISSN:	0304-3835 1872-7980
DOI:	10.1016/j.canlet.2013.02.048