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- W2225768615 abstract "Progression of epithelial tumor cells to the invasive and metastatic phenotype requires increased cellular plasticity of the tumor cell. This plasticity allows tumor cells to invade locally and into neighboring organs, penetrate blood vessels, and metastasize to distant organs. Metastasizing tumor cells show increased migratory capacity and altered matrix degradation and deposition. A partial loss of epithelial cell fate differentiation and a gain of mesenchymal characteristics has been described as epithelial-mesenchymal transition (EMT) of tumor cells. EMT allows epithelial derived tumor cells, similar to mesenchymal cells, to migrate on and invade in mesenchymal extra-cellular matrix (ECM) of the tumor stroma and into blood vessels, and metastasize. TGFβ plays a complex role during the development of carcinoma formation and cancer progression. While untransformed cells and early steps of tumor formation are often inhibited in proliferation by TGFβ later stages of tumor progression are positively regulated by TGFβ Accordingly, elements of TGFβ signal transduction are mutated in some tumor types while TGFβ signaling is maintained and activated in the majority of other tumors. TGFβ positively regulates many aspects of tumor progression such as extracellular matrix regulation, cell invasion, angiogenesis, immune suppression and, most notably, EMT of tumor cells. EMT induced by TGFβ has been found to be essential for tumor invasion metastasis. Accordingly, clinical evidence reveals TGFβ as a major risk factor for tumor progression. Here I review both TGFβ signaling in tumor suppression as well as the increasing evidence linking TGFβ to tumor progression, invasion and metastasis." @default.
- W2225768615 created "2016-06-24" @default.
- W2225768615 creator A5021268908 @default.
- W2225768615 date "2006-01-18" @default.
- W2225768615 modified "2023-10-18" @default.
- W2225768615 title "TGFβ Receptor Signaling in Cancer and Metastasis" @default.
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